diff --git a/_quarto.yml b/_quarto.yml index da36b7f..f905647 100644 --- a/_quarto.yml +++ b/_quarto.yml @@ -3,13 +3,16 @@ project: website: title: "LNSC Browser" + navbar: search: true left: - - projects.qmd + - text: Projects + file: projects.qmd - atlases.qmd - pubs.qmd - investigators.qmd + search: location: navbar type: textbox @@ -19,6 +22,7 @@ format: theme: darkly css: styles.css toc: true + toc-depth: 1 editor: visual diff --git a/atlases/2021-walsh/2021-walsh.jpg b/atlases/2021-walsh/2021-walsh.jpg deleted file mode 100644 index 54d3e97..0000000 Binary files a/atlases/2021-walsh/2021-walsh.jpg and /dev/null differ diff --git a/atlases/2021-walsh/index.qmd b/atlases/2021-walsh/index.qmd index bf4c21e..53c53fd 100644 --- a/atlases/2021-walsh/index.qmd +++ b/atlases/2021-walsh/index.qmd @@ -1,7 +1,9 @@ --- title: Molecular tracking devices quantify antigen distribution and archiving in the murine lymph node -image: 2021-walsh.jpg -categories: [project-2, core-c, core-d] +image: /images/2021-walsh.jpg +date: 'April 12, 2021' + +categories: [project-2, core-b, core-c, core-d] about: id: about template: jolla diff --git a/authors.yml b/authors.yml index 322aeba..db5617d 100644 --- a/authors.yml +++ b/authors.yml @@ -1,10 +1,3 @@ -Ryan Sheridan: - suffix: PhD - links: - publications: https://orcid.org/0000-0003-4012-3147 - website: https://github.com/sheridar - email: mailto:ryan.sheridan@cuanschutz.edu - project: core-d Thomas Morrison: suffix: PhD links: @@ -40,7 +33,9 @@ Beth Tamburini: links: website: https://medschool.cuanschutz.edu/gastroenterology/research/research-laboratories/beth-jiron-tamburini-lab email: mailto:beth.tamburini@cuanschutz.edu - project: project-2 + project: + - project-2 + - core-b bio: The overarching goal of my research program is to understand how the lymphatic stroma recognize and react to stimuli within the lymph to guide the immune response. My initial studies of lymphatic stroma were focused on understanding the mechanisms @@ -59,6 +54,7 @@ Beth Tamburini: in developing this research program. This collaborative research program as proven to be well suited for the training and success of the graduate students and post-docs in my laboratory. + image: /home/rmsheridan/Projects/lnsc-cell-browser/images/beth-tamburini.jpg Jenna Guthmiller: suffix: PhD links: @@ -88,6 +84,7 @@ Jenna Guthmiller: conserved, albeit non-protective antigens. Together, these studies highlight the importance of understanding how preexisting antibodies influence the generation of broadly protective immunity. + image: /home/rmsheridan/Projects/lnsc-cell-browser/images/jenna-guthmiller.jpeg Jay Hesselberth: suffix: PhD links: @@ -110,6 +107,13 @@ Jay Hesselberth: et al.). More recently, we have applied nanopore RNA sequencing to characterize the landscape of RNA repair events in budding yeast. image: /home/rmsheridan/Projects/lnsc-cell-browser/images/jay-hesselberth.png +Ryan Sheridan: + suffix: PhD + links: + publications: https://orcid.org/0000-0003-4012-3147 + website: https://github.com/sheridar + email: mailto:ryan.sheridan@cuanschutz.edu + project: core-d Jennifer Matsuda: suffix: PhD links: @@ -161,3 +165,22 @@ Nicholas May: [] Heather Hickman: [] Tadg Forward: [] Aspen Martin: [] +Susan Elmore: [] +Tonya Colpitts: [] +Austin Gillen: [] +Michael Kriss: [] +Kent Riemondy: [] +Ronald Schuyler: [] +Hugo Rosen: [] +Madison Kraus: [] +Ira Fleming: [] +Aspen Uecker-Martin: [] +Ju-Sim Kim: [] +Lin Liu: [] +Sashi Kant: [] +David Orlicky: [] +Siva Uppalapati: [] +Alyssa Margolis: [] +Michael McClelland: [] +Jessica Jones-Carson: [] +Andres Vazquez-Torres: [] diff --git a/funs.R b/funs.R index 7b62521..dd0b76a 100644 --- a/funs.R +++ b/funs.R @@ -82,12 +82,20 @@ # Set publication key based on first author and key # this is used to create page directories - yr <- html %>% + date <- html %>% html_element("span.cit") %>% html_text2() %>% - str_extract("^[0-9]{4}(?= )") + str_extract("^[^;]+") - if (is.na(yr)) cli_abort("Error extracting year from pubmed link") + if (is.na(date)) cli_abort("Error extracting date from pubmed link") + + date <- date %>% + as.Date(format = "%Y %b %d") + + yr <- year(date) + + date <- date %>% + format("%B %d, %Y") athr1 <- athrs[1] %>% str_extract("[^ ]+$") %>% @@ -99,6 +107,7 @@ res <- list( key = key, title = ttl, + date = date, year = yr, authors = athrs, abstract = abst diff --git a/images/2014-tamburini.jpg b/images/2014-tamburini.jpg new file mode 100644 index 0000000..69b0f40 Binary files /dev/null and b/images/2014-tamburini.jpg differ diff --git a/images/2018-lucas.jpg b/images/2018-lucas.jpg new file mode 100644 index 0000000..cb249a2 Binary files /dev/null and b/images/2018-lucas.jpg differ diff --git a/images/2018-mccarthy.jpg b/images/2018-mccarthy.jpg new file mode 100644 index 0000000..686972b Binary files /dev/null and b/images/2018-mccarthy.jpg differ diff --git a/images/2019-tamburini.jpg b/images/2019-tamburini.jpg new file mode 100644 index 0000000..804d4c6 Binary files /dev/null and b/images/2019-tamburini.jpg differ diff --git a/images/2020-lucas.jpg b/images/2020-lucas.jpg new file mode 100644 index 0000000..c17109d Binary files /dev/null and b/images/2020-lucas.jpg differ diff --git a/images/2023-tamburini.jpg b/images/2023-tamburini.jpg new file mode 100644 index 0000000..8b526f2 Binary files /dev/null and b/images/2023-tamburini.jpg differ diff --git a/images/beth-tamburini.jpg b/images/beth-tamburini.jpg new file mode 100644 index 0000000..e2c4be8 Binary files /dev/null and b/images/beth-tamburini.jpg differ diff --git a/images/jenna-guthmiller.jpeg b/images/jenna-guthmiller.jpeg new file mode 100644 index 0000000..bba0b04 Binary files /dev/null and b/images/jenna-guthmiller.jpeg differ diff --git a/images/pub_tl.png b/images/pub_tl.png new file mode 100644 index 0000000..6aa6139 Binary files /dev/null and b/images/pub_tl.png differ diff --git a/images/thomas-morrison-2.png b/images/thomas-morrison-2.png new file mode 100644 index 0000000..e3e2c70 Binary files /dev/null and b/images/thomas-morrison-2.png differ diff --git a/images/thomas-morrison.png b/images/thomas-morrison.png index e3e2c70..e549587 100644 Binary files a/images/thomas-morrison.png and b/images/thomas-morrison.png differ diff --git a/index.qmd b/index.qmd index ed441af..a96a478 100644 --- a/index.qmd +++ b/index.qmd @@ -14,31 +14,51 @@ library(here) source(here("funs.R")) +# Read yamls proj_yml <- read_yaml(here("projects.yml")) pub_yml <- read_yaml(here("pubs.yml")) athr_yml <- read_yaml(here("authors.yml")) lnk_cls <- "{.link-box}" +# Create links for each project links <- .create_project_links(proj_yml, athr_yml, pub_yml, lnk_cls) +# Split into projects and cores +# maintain order provided in yaml +proj_type <- proj_yml %>% + names() %>% + str_extract("^[^-]+") %>% + str_to_title() %>% + str_c("s") %>% + factor(levels = unique(.)) + +proj_yml <- proj_yml %>% + split(proj_type) + +# Create section text text <- proj_yml %>% imap(~ { - ttl_lnk <- .x$title %>% - str_to_lower() %>% - str_replace_all("( |, )", "-") %>% - str_c("[", .x$title, "](projects.qmd#", ., "){.bold-link}") + ttl <- str_c("## ", .y, "\n\n") - str_c( - "* ", ttl_lnk, " \n", - links[[.y]], " \n", - .x$short, "\n\n" - ) + .x %>% + imap(~ { + ttl_lnk <- .x$title %>% + str_to_lower() %>% + str_replace_all("( |, )", "-") %>% + str_c("[", .x$title, "](projects.qmd#", ., "){.bold-link}") + + str_c( + "* ", ttl_lnk, " \n", + links[[.y]], " \n", + .x$short, "\n\n" + ) + }) %>% + str_c(collapse = "") %>% + str_c(ttl, .) }) %>% str_c(collapse = "") ``` -The theme uniting our program is that lymph node stromal cells (LNSC)s are an understudied and untapped source of immunomodulatory control. LNSCs are comprised of diverse populations of fibroblasts and endothelial cells. LNSCs coordinate lymphocyte entry into the lymph node (LN), facilitate lymphocyte trafficking into distinct LN niches, regulate lymphocyte survival, and promote LN expansion. Our overall hypothesis is that viral and antigen acquisition by LNSCs shapes immunity by programming pathogen and vaccine specific responses, and that LNSCs can be manipulated by pathogens and vaccines to guide immune outcomes. - -## Projects +Lymph node stromal cells (LNSC)s are an understudied and untapped source of immunomodulatory control. LNSCs are comprised of diverse populations of fibroblasts and endothelial cells. LNSCs coordinate lymphocyte entry into the lymph node (LN), facilitate lymphocyte trafficking into distinct LN niches, regulate lymphocyte survival, and promote LN expansion. The goal of this program is to investigate how viral and antigen acquisition by LNSCs shape immunity and how LNSCs can be manipulated by pathogens and vaccines to guide immune outcomes. `r text` diff --git a/investigators.qmd b/investigators.qmd index ffdcad8..73898de 100644 --- a/investigators.qmd +++ b/investigators.qmd @@ -34,7 +34,7 @@ text <- athr_yml %>% if (!is.null(.x$suffix)) sfx <- str_c(", ", .x$suffix) res <- str_c( - "## ", .y, sfx, "\n\n", + "

", .y, sfx, "

\n\n", lnks, "\n\n", .x$bio, "\n\n" ) @@ -45,14 +45,10 @@ text <- athr_yml %>% html_head <- str_c( "
\n", - " \n", - "

\n" + " \n" ) - html_foot <- str_c( - "

\n", - "
" - ) + html_foot <- "" res <- str_c( html_head, res, diff --git a/pre-build.R b/pre-build.R index 9a94622..c889df7 100644 --- a/pre-build.R +++ b/pre-build.R @@ -1,7 +1,7 @@ # Run this script prior to building site to: # * Scrape publication information and generate publication pages # * Update authors.yml based on publication information -# * Serach for author images and update authors.yml +# * Search for author images and update authors.yml library(yaml) library(tidyverse) @@ -45,8 +45,13 @@ link_info <- list( # Template to write index.qmd index_qmd <- "---\ntitle: {ttl}\n" +# Check for duplicated publications +dup_pubs <- pub_yml %>% + map_chr(pluck, "pubmed") %>% + duplicated() + # Create index.qmd for each pub entry -pub_yml_new <- pub_yml %>% +pub_yml_new <- pub_yml[!dup_pubs] %>% imap(~ { pub_info <- .x @@ -55,7 +60,7 @@ pub_yml_new <- pub_yml %>% # Scrape missing info from pubmed pub_attrs <- c( - "key", "title", "year", + "key", "title", "date", "year", "authors", "abstract", "image" ) @@ -91,7 +96,7 @@ pub_yml_new <- pub_yml %>% if (length(img) > 1) img <- img[[1]] - } else if (file.exists(pub_info$image)) { + } else if (file.exists(str_remove(pub_info$image, "^/"))) { img <- pub_info$image } else { @@ -102,20 +107,18 @@ pub_yml_new <- pub_yml %>% download.file(img_dwnld, img) } - img_nm <- basename(img) - img_lnk <- here(pub, img_nm) + img <- str_remove(img, here()) # image path should be relative to site # Conditionally add image field to index.qmd - if (!is_empty(img_lnk)) { - index_qmd <- str_c(index_qmd, "image: {img_nm}\n") - - if (!file.exists(img_lnk)) file.link(img, img_lnk) + if (!is_empty(img)) { + index_qmd <- str_c(index_qmd, "image: {img}\n") - pub_info$image <- img_lnk + pub_info$image <- img } index_qmd <- str_c( index_qmd, + "date: '{pub_info$date}'\n\n", "categories: [{cats_str}]\n", "about:\n", " id: about\n", @@ -198,7 +201,7 @@ pub_yml_new <- pub_yml %>% # Write updated pubs.yml # this will have info scraped from pubmed if (!identical(pub_yml, pub_yml_new)) { - pub_yml %>% + pub_yml_new %>% write_yaml(here("pubs.yml")) } @@ -230,6 +233,83 @@ athr_yml_new <- athr_yml %>% }) if (!identical(athr_yml, athr_yml_new)) { - athr_yml %>% + athr_yml_new %>% write_yaml(here("authors.yml")) } + + +# TIMELINE ---- + +# Filter for authors to label +lab_athr <- athr_yml_new %>% + keep(~ !is.null(.x$project)) %>% + names() + +tl_dat <- pub_yml_new %>% + map_dfr(~ { + athrs <- .x$authors + athrs <- athrs[athrs %in% lab_athr] + athrs <- str_extract(athrs, "[^ ]+$") + + tibble( + key = .x$key, + date = as.Date(str_c(.x$year, "-01-01")), + authors = str_c(athrs, collapse = ", "), + pmid = str_extract(.x$pubmed, "[0-9]+(/|)$") + ) + }) + +# Format publication data +tl_dat <- tl_dat %>% + mutate( + authors = str_wrap(authors, width = 10), + pmid = str_remove(pmid, "/$"), + pmid = str_c("PMID ", pmid), + lab = str_c(authors, "\n", pmid), + year = as.character(year(date)) + ) %>% + group_by(date, year) %>% + summarize(lab = str_c(lab, collapse = "\n\n"), .groups = "drop") + +# Create publication timeline +tl <- tl_dat %>% + ggplot(aes(date, 0)) + + geom_line( + linewidth = 3 + ) + + geom_point( + # shape = 25, + size = 6, + fill = "black" + ) + + geom_text( + aes(y = 0.35, label = year), + size = 24 / .pt, + color = "white" + # fontface = "bold" + ) + + geom_text( + aes(y = -0.25, label = lab), + hjust = 0, + vjust = 1, + size = 12 / .pt, + color = "white" + # fontface = "italic" + ) + + coord_cartesian( + xlim = c(min(tl_dat$date), max(tl_dat$date) + years(1)), + ylim = c(-3, 0.6) + ) + + theme_void() + + theme( + plot.background = element_rect(fill = "#303030", color = "#303030") + ) + +ggsave( + tl, + filename = here(img_dir, "pub_tl.png"), + width = 18, + height = 5, + dpi = 300, + device = "png" +) diff --git a/projects.qmd b/projects.qmd index 46424c5..ab05eb6 100644 --- a/projects.qmd +++ b/projects.qmd @@ -1,5 +1,7 @@ --- -title: "Projects" +html: + toc: false + toc-depth: 2 --- ```{r, echo = FALSE, include = FALSE} @@ -9,31 +11,51 @@ library(here) source(here("funs.R")) +# Read yamls proj_yml <- read_yaml(here("projects.yml")) athr_yml <- read_yaml(here("authors.yml")) pub_yml <- read_yaml(here("pubs.yml")) lnk_cls <- "{.link-box}" +# Create project links links <- .create_project_links(proj_yml, athr_yml, pub_yml, lnk_cls) +# maintain order provided in yaml +proj_type <- proj_yml %>% + names() %>% + str_extract("^[^-]+") %>% + str_to_title() %>% + str_c("s") %>% + factor(levels = unique(.)) + +proj_yml <- proj_yml %>% + split(proj_type) + text <- proj_yml %>% imap(~ { - ttl_lnk <- .x$title %>% - str_to_lower() %>% - str_replace_all("( |, )", "-") %>% - str_c("[", .x$title, "](projects.qmd#", ., "){.bold-link}") - - # Conditional add hypothesis - hyp <- .x$hypothesis - - if (!is.null(hyp)) str_c("*", hyp, "*\n\n") + ttl <- str_c("# ", .y, "\n\n") - str_c( - "## ", .x$title, "\n\n", - links[[.y]], "\n\n", - hyp, - .x$abstract, "\n\n" - ) + .x %>% + imap(~ { + ttl_lnk <- .x$title %>% + str_to_lower() %>% + str_replace_all("( |, )", "-") %>% + str_c("[", .x$title, "](projects.qmd#", ., "){.bold-link}") + + # Conditional add hypothesis + hyp <- .x$hypothesis + + if (!is.null(hyp)) str_c("*", hyp, "*\n\n") + + str_c( + "## ", .x$title, "\n\n", + links[[.y]], "\n\n", + hyp, + .x$abstract, "\n\n" + ) + }) %>% + str_c(collapse = "") %>% + str_c(ttl, .) }) %>% str_c(collapse = "") ``` diff --git a/projects.yml b/projects.yml index 2feaed1..c4b578c 100644 --- a/projects.yml +++ b/projects.yml @@ -16,7 +16,17 @@ project-3: hypothesis: We hypothesize that antibody isotype in an IC regulates protective immunity by determining which LNSC populations acquire and retain antigen via isotype-specific interactions with complement and Fc receptors (FcRs) abstract: Project 3 will engineer monoclonal antibodies (mAbs) with fixed antigen specificity on discrete antibody isotypes and subclasses. Using stabilized DNA conjugates, Projects 2 and 3 will track antibody:antigen complexes to determine the spatial and cellular localization of ICs in comparison with free antigen. Project 3 also investigates how FcR expression by LNSCs impacts IC acquisition and will work with Project 1 to determine viral antigen retention and define consequences to protective humoral and cellular immunity. This project uses mouse models engineered to manipulate complement receptor and FcR expression by discrete LNSC populations (Core B) and addresses the Program hypothesis by defining how different LNSC populations use antibody to determine antigen uptake and localization. +core-b: + title: Animal and tissue core + short: The goal of the animal and tissue core is to generate novel genetic mouse models and to develop a tissue and cell repository + abstract: The goal of the animal and tissue core is to generate novel genetic mouse models and to develop a tissue and cell repository + core-c: - title: Core C - Molecular Technologies - short: The molecular technologies cores will apply new molecular tools to understand the contributions of lymph node stromal cells (LNSC) to immune responses + title: Molecular technologies core + short: The molecular technologies core will apply new molecular tools to understand the contributions of lymph node stromal cells (LNSC) to immune responses abstract: The molecular technologies cores will apply new molecular tools to understand the contributions of lymph node stromal cells (LNSC) to immune responses + +core-d: + title: Bioinformatics core + short: The bioinformatics core will apply new informatics approaches to understand the contributions of lymph node stromal cells (LN SC) to immune responses + abstract: The bioinformatics core will apply new informatics approaches to understand the contributions of lymph node stromal cells (LN SC) to immune responses diff --git a/pubs.qmd b/pubs.qmd index 8b1a22d..a42be60 100644 --- a/pubs.qmd +++ b/pubs.qmd @@ -2,9 +2,14 @@ title: "Publications" listing: contents: "pubs/*/index.qmd" + sort: + - "date desc" + - "title" type: grid categories: numbered feed: false - fields: [image, title] + fields: [image, title, date] page-layout: full +description: | + ![](/images/pub_tl.png) --- diff --git a/pubs.yml b/pubs.yml index 1ca59b3..2388f44 100644 --- a/pubs.yml +++ b/pubs.yml @@ -32,11 +32,13 @@ enable new approaches to study dynamic tissue dissemination of antigen-adjuvant conjugates and identify new mechanisms of antigen acquisition and retention at cellular resolution in vivo. - image: /home/rmsheridan/Projects/lnsc-cell-browser/pubs/2021-walsh/2021-walsh.jpg + image: /images/2021-walsh.jpg project: - project-2 + - core-b - core-c - core-d + date: April 12, 2021 - pubmed: https://pubmed.ncbi.nlm.nih.gov/29229919/ key: 2017-kedl title: Migratory dendritic cells acquire and present lymphatic endothelial cell-archived @@ -62,8 +64,11 @@ migratory DCs potentially acquiring apoptotic LECs. In conclusion, LEC-archived antigens are exchanged with migratory DCs, both directly and through LEC apoptosis, to cross-present archived antigens to circulating T cells. - image: /home/rmsheridan/Projects/lnsc-cell-browser/pubs/2017-kedl/2017-kedl.jpg - project: project-2 + image: /images/2017-kedl.jpg + project: + - project-2 + - core-b + date: December 11, 2017 - pubmed: https://pubmed.ncbi.nlm.nih.gov/34618370/ links: github: https://github.com/rnabioco/morrison-chikv @@ -103,51 +108,14 @@ unrecognized arbovirus-scavenging role for lymphatic endothelial cells and improve our mechanistic understanding of viremia control during arthritogenic alphavirus infection. - image: /home/rmsheridan/Projects/lnsc-cell-browser/pubs/2021-carpentier/2021-carpentier.jpg + image: /images/2021-carpentier.jpg project: - project-1 - project-2 + - core-b - core-c - core-d -- pubmed: https://pubmed.ncbi.nlm.nih.gov/33843587/ - links: - github: https://github.com/rnabioco/antigen-tracking - atlas: https://d3898ys7yh3545.cloudfront.net/ - geo: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150719 - key: 2021-walsh - title: Molecular tracking devices quantify antigen distribution and archiving in - the murine lymph node - year: '2021' - authors: - - Shannon Walsh - - Ryan Sheridan - - Erin Lucas - - Thu Doan - - Brian Ware - - Johnathon Schafer - - Rui Fu - - Matthew Burchill - - Jay Hesselberth - - Beth Tamburini - abstract: The detection of foreign antigens in vivo has relied on fluorescent conjugation - or indirect read-outs such as antigen presentation. In our studies, we found that - these widely used techniques had several technical limitations that have precluded - a complete picture of antigen trafficking or retention across lymph node cell - types. To address these limitations, we developed a 'molecular tracking device' - to follow the distribution, acquisition, and retention of antigen in the lymph - node. Utilizing an antigen conjugated to a nuclease-resistant DNA tag, acting - as a combined antigen-adjuvant conjugate, and single-cell mRNA sequencing, we - quantified antigen abundance in the lymph node. Variable antigen levels enabled - the identification of caveolar endocytosis as a mechanism of antigen acquisition - or retention in lymphatic endothelial cells. Thus, these molecular tracking devices - enable new approaches to study dynamic tissue dissemination of antigen-adjuvant - conjugates and identify new mechanisms of antigen acquisition and retention at - cellular resolution in vivo. - image: /home/rmsheridan/Projects/lnsc-cell-browser/pubs/2021-walsh/2021-walsh.jpg - project: - - project-2 - - core-c - - core-d + date: November 15, 2021 - pubmed: https://pubmed.ncbi.nlm.nih.gov/35505125/ key: 2022-doan title: Trafficking and retention of protein antigens across systems and immune cell @@ -171,8 +139,11 @@ protective immune responses. Therefore, understanding antigen trafficking and retention is necessary to understand the type and magnitude of the immune response and essential for the development of novel vaccine and therapeutic targets. - image: /home/rmsheridan/Projects/lnsc-cell-browser/pubs/2022-doan/2022-doan.jpg - project: project-2 + image: /images/2022-doan.jpg + project: + - project-2 + - core-b + date: May 03, 2022 - pubmed: https://pubmed.ncbi.nlm.nih.gov/38194268/ key: 2024-lucas title: Chikungunya virus infection disrupts lymph node lymphatic endothelial cell @@ -206,5 +177,251 @@ project: - project-1 - project-2 + - core-b - core-c - core-d + date: January 09, 2024 +- pubmed: https://pubmed.ncbi.nlm.nih.gov/29997290/ + key: 2018-mccarthy + title: Chikungunya virus impairs draining lymph node function by inhibiting HEV-mediated + lymphocyte recruitment + year: '2018' + authors: + - Mary McCarthy + - Bennett Davenport + - Glennys Reynoso + - Erin Lucas + - Nicholas May + - Susan Elmore + - Beth Tamburini + - Heather Hickman + - Thomas Morrison + abstract: Chikungunya virus (CHIKV) causes acute and chronic rheumatologic disease. + Pathogenic CHIKV strains persist in joints of immunocompetent mice, while the + attenuated CHIKV strain 181/25 is cleared by adaptive immunity. We analyzed the + draining lymph node (dLN) to define events in lymphoid tissue that may contribute + to CHIKV persistence or clearance. Acute 181/25 infection resulted in dLN enlargement + and germinal center (GC) formation, while the dLN of mice infected with pathogenic + CHIKV became highly disorganized and depleted of lymphocytes. Using CHIKV strains + encoding ovalbumin-specific TCR epitopes, we found that lymphocyte depletion was + not due to impaired lymphocyte proliferation. Instead, the accumulation of naive + lymphocytes transferred from the vasculature to the dLN was reduced, which was + associated with fewer high endothelial venule cells and decreased CCL21 production. + Following NP-OVA immunization, NP-specific GC B cells in the dLN were decreased + during pathogenic, but not attenuated, CHIKV infection. Our data suggest that + pathogenic, persistent strains of CHIKV disable the development of adaptive immune + responses within the dLN. + image: /images/2018-mccarthy.jpg + project: + - project-1 + - project-2 + - core-b + date: July 12, 2018 +- pubmed: https://pubmed.ncbi.nlm.nih.gov/30045970/ + key: 2018-lucas + title: Type 1 IFN and PD-L1 Coordinate Lymphatic Endothelial Cell Expansion and + Contraction during an Inflammatory Immune Response + year: '2018' + authors: + - Erin Lucas + - Jeffrey Finlon + - Matthew Burchill + - Mary McCarthy + - Thomas Morrison + - Tonya Colpitts + - Beth Tamburini + abstract: Lymph node (LN) expansion during an immune response is a complex process + that involves the relaxation of the fibroblastic network, germinal center formation, + and lymphatic vessel growth. These processes require the stromal cell network + of the LN to act deliberately to accommodate the influx of immune cells to the + LN. The molecular drivers of these processes are not well understood. Therefore, + we asked whether the immediate cytokines type 1 IFN produced during viral infection + influence the lymphatic network of the LN in mice. We found that following an + IFN-inducing stimulus such as viral infection or polyI:C, programmed cell death + ligand 1 (PD-L1) expression is dynamically upregulated on lymphatic endothelial + cells (LECs). We found that reception of type 1 IFN by LECs is important for the + upregulation of PD-L1 of mouse and human LECs and the inhibition of LEC expansion + in the LN. Expression of PD-L1 by LECs is also important for the regulation of + LN expansion and contraction after an IFN-inducing stimulus. We demonstrate a + direct role for both type 1 IFN and PD-L1 in inhibiting LEC division and in promoting + LEC survival. Together, these data reveal a novel mechanism for the coordination + of type 1 IFN and PD-L1 in manipulating LEC expansion and survival during an inflammatory + immune response. + image: /images/2018-lucas.jpg + project: + - project-1 + - project-2 + - core-b + date: September 15, 2018 +- pubmed: https://pubmed.ncbi.nlm.nih.gov/31156626/ + key: 2019-tamburini + title: Chronic Liver Disease in Humans Causes Expansion and Differentiation of Liver + Lymphatic Endothelial Cells + year: '2019' + authors: + - Beth Tamburini + - Jeffrey Finlon + - Austin Gillen + - Michael Kriss + - Kent Riemondy + - Rui Fu + - Ronald Schuyler + - Jay Hesselberth + - Hugo Rosen + - Matthew Burchill + abstract: Liver lymphatic vessels support liver function by draining interstitial + fluid, cholesterol, fat, and immune cells for surveillance in the liver draining + lymph node. Chronic liver disease is associated with increased inflammation and + immune cell infiltrate. However, it is currently unknown if or how lymphatic vessels + respond to increased inflammation and immune cell infiltrate in the liver during + chronic disease. Here we demonstrate that lymphatic vessel abundance increases + in patients with chronic liver disease and is associated with areas of fibrosis + and immune cell infiltration. Using single-cell mRNA sequencing and multi-spectral + immunofluorescence analysis we identified liver lymphatic endothelial cells and + found that chronic liver disease results in lymphatic endothelial cells (LECs) + that are in active cell cycle with increased expression of CCL21. Additionally, + we found that LECs from patients with NASH adopt a transcriptional program associated + with increased IL13 signaling. Moreover, we found that oxidized low density lipoprotein, + associated with NASH pathogenesis, induced the transcription and protein production + of IL13 in LECs both in vitro and in a mouse model. Finally, we show that oxidized + low density lipoprotein reduced the transcription of PROX1 and decreased lymphatic + stability. Together these data indicate that LECs are active participants in the + liver, expanding in an attempt to maintain tissue homeostasis. However, when inflammatory + signals, such as oxidized low density lipoprotein are increased, as in NASH, lymphatic + function declines and liver homeostasis is impeded. + image: /images/2019-tamburini.jpg + project: + - project-2 + - core-b + - core-c + - core-d + date: May 15, 2019 +- pubmed: https://pubmed.ncbi.nlm.nih.gov/33053342/ + key: 2020-lucas + title: PD-L1 Reverse Signaling in Dermal Dendritic Cells Promotes Dendritic Cell + Migration Required for Skin Immunity + year: '2020' + authors: + - Erin Lucas + - Johnathon Schafer + - Jennifer Matsuda + - Madison Kraus + - Matthew Burchill + - Beth Tamburini + abstract: Although the function of the extracellular region of programmed death + ligand 1 (PD-L1) through its interactions with PD-1 on T cells is well studied, + little is understood regarding the intracellular domain of PD-L1. Here, we outline + a major role for PD-L1 intracellular signaling in the control of dendritic cell + (DC) migration from the skin to the draining lymph node (dLN). Using a mutant + mouse model, we identify a TSS signaling motif within the intracellular domain + of PD-L1. The TSS motif proves critical for chemokine-mediated DC migration to + the dLN during inflammation. This loss of DC migration, in the PD-L1 TSS mutant, + leads to a significant decline in T cell priming when DC trafficking is required + for antigen delivery to the dLN. Finally, the TSS motif is required for chemokine + receptor signaling downstream of the Gα subunit of the heterotrimeric G protein + complex, ERK phosphorylation, and actin polymerization in DCs. + image: /images/2020-lucas.jpg + project: + - project-2 + - core-b + date: October 13, 2020 +- pubmed: https://pubmed.ncbi.nlm.nih.gov/37841845/ + key: 2023-tamburini + title: Vaccine-induced antigen archiving enhances local memory CD8+ T cell responses + following an unrelated viral infection + year: '2023' + authors: + - Beth Tamburini + - Thu Doan + - Tadg Forward + - Erin Lucas + - Ira Fleming + - Aspen Uecker-Martin + - Jay Hesselberth + - Thomas Morrison + abstract: Viral and vaccine antigens persist or are archived in lymph node stromal + cells (LNSC) such as lymphatic endothelial cells (LEC) and fibroblastic reticular + cells (FRC). Here, we find that, during the time frame of antigen archiving, LEC + apoptosis caused by a second, but unrelated, innate immune stimulus such as vaccina + viral infection or CpG DNA administration boosted memory CD8+ T cells specific + to the archived antigen. In contrast to "bystander" activation associated with + unrelated infections, the memory CD8+ T cells specific to the vaccine archived + antigen were significantly higher than memory CD8+ T cells of a different antigen + specificity. Finally, the boosted memory CD8+ T cells resulted in increased protection + against Listeria monocytogenes expressing the vaccine antigen, but only for the + duration that the vaccine antigen was archived. These findings outline a novel + mechanism by which LNSC archived antigens, in addition to bystander activation, + can augment memory CD8+ T cell responses during repeated inflammatory insults. + image: /images/2023-tamburini.jpg + project: + - project-1 + - project-2 + - core-b + - core-c + - core-d + date: September 25, 2023 +- pubmed: https://pubmed.ncbi.nlm.nih.gov/38307020/ + key: 2024-kim + title: Anaerobic respiration of host-derived methionine sulfoxide protects intracellular + Salmonella from the phagocyte NADPH oxidase + year: '2024' + authors: + - Ju-Sim Kim + - Lin Liu + - Sashi Kant + - David Orlicky + - Siva Uppalapati + - Alyssa Margolis + - Bennett Davenport + - Thomas Morrison + - Jennifer Matsuda + - Michael McClelland + - Jessica Jones-Carson + - Andres Vazquez-Torres + abstract: Intracellular Salmonella experiencing oxidative stress downregulates aerobic + respiration. To maintain cellular energetics during periods of oxidative stress, + intracellular Salmonella must utilize terminal electron acceptors of lower energetic + value than molecular oxygen. We show here that intracellular Salmonella undergoes + anaerobic respiration during adaptation to the respiratory burst of the phagocyte + NADPH oxidase in macrophages and in mice. Reactive oxygen species generated by + phagocytes oxidize methionine, generating methionine sulfoxide. Anaerobic Salmonella + uses the molybdenum cofactor-containing DmsABC enzymatic complex to reduce methionine + sulfoxide. The enzymatic activity of the methionine sulfoxide reductase DmsABC + helps Salmonella maintain an alkaline cytoplasm that supports the synthesis of + the antioxidant hydrogen sulfide via cysteine desulfuration while providing a + source of methionine and fostering redox balancing by associated dehydrogenases. + Our investigations demonstrate that nontyphoidal Salmonella responding to oxidative + stress exploits the anaerobic metabolism associated with dmsABC gene products, + a pathway that has accrued inactivating mutations in human-adapted typhoidal serovars. + project: + - project-1 + - core-b + date: January 24, 2024 +- pubmed: https://pubmed.ncbi.nlm.nih.gov/24905362/ + key: 2014-tamburini + title: Antigen capture and archiving by lymphatic endothelial cells following vaccination + or viral infection + date: June 06, 2014 + year: 2014.0 + authors: + - Beth Tamburini + - Matthew Burchill + - Ross Kedl + abstract: Antigen derived from viral infections with influenza and vesicular stomatitis + virus can persist after resolution of infection. Here we show that antigen can + similarly persist for weeks following viral challenge and vaccination. Antigen + is captured by lymphatic endothelial cells (LECs) under conditions that induce + LEC proliferation. Consistent with published data showing that viral antigen persistence + impacts the function of circulating memory T cells, we find that vaccine-elicited + antigen persistence, found on LECs, positively influences the degree of protective + immunity provided by circulating memory CD8(+) T cells. The coupling of LEC proliferation + and antigen capture identifies a mechanism by which the LECs store, or 'archive', + antigens for extended periods of time after antigen challenge, thereby increasing + IFNγ/IL-2 production and enhancing protection against infection. These findings + therefore have the potential to have an impact on future vaccination strategies + and our understanding of the role for persisting antigen in both vaccine and infectious + settings. + image: /images/2014-tamburini.jpg + project: + - project-2 + - core-b diff --git a/pubs/2014-tamburini/index.qmd b/pubs/2014-tamburini/index.qmd new file mode 100644 index 0000000..3f50cc7 --- /dev/null +++ b/pubs/2014-tamburini/index.qmd @@ -0,0 +1,18 @@ +--- +title: Antigen capture and archiving by lymphatic endothelial cells following vaccination or viral infection +image: /images/2014-tamburini.jpg +date: 'June 06, 2014' + +categories: [project-2, core-b] +about: + id: about + template: jolla + links: + - text: Publication + icon: file-earmark + href: https://pubmed.ncbi.nlm.nih.gov/24905362/ +--- + +Beth Tamburini, Matthew Burchill, Ross Kedl + +Antigen derived from viral infections with influenza and vesicular stomatitis virus can persist after resolution of infection. Here we show that antigen can similarly persist for weeks following viral challenge and vaccination. Antigen is captured by lymphatic endothelial cells (LECs) under conditions that induce LEC proliferation. Consistent with published data showing that viral antigen persistence impacts the function of circulating memory T cells, we find that vaccine-elicited antigen persistence, found on LECs, positively influences the degree of protective immunity provided by circulating memory CD8(+) T cells. The coupling of LEC proliferation and antigen capture identifies a mechanism by which the LECs store, or 'archive', antigens for extended periods of time after antigen challenge, thereby increasing IFNγ/IL-2 production and enhancing protection against infection. These findings therefore have the potential to have an impact on future vaccination strategies and our understanding of the role for persisting antigen in both vaccine and infectious settings. diff --git a/pubs/2017-kedl/2017-kedl.jpg b/pubs/2017-kedl/2017-kedl.jpg deleted file mode 100644 index d410975..0000000 Binary files a/pubs/2017-kedl/2017-kedl.jpg and /dev/null differ diff --git a/pubs/2017-kedl/index.qmd b/pubs/2017-kedl/index.qmd index d9f4f79..bba920f 100644 --- a/pubs/2017-kedl/index.qmd +++ b/pubs/2017-kedl/index.qmd @@ -1,7 +1,9 @@ --- title: Migratory dendritic cells acquire and present lymphatic endothelial cell-archived antigens during lymph node contraction -image: 2017-kedl.jpg -categories: [project-2] +image: /images/2017-kedl.jpg +date: 'December 11, 2017' + +categories: [project-2, core-b] about: id: about template: jolla diff --git a/pubs/2018-lucas/index.qmd b/pubs/2018-lucas/index.qmd new file mode 100644 index 0000000..6f6da83 --- /dev/null +++ b/pubs/2018-lucas/index.qmd @@ -0,0 +1,18 @@ +--- +title: Type 1 IFN and PD-L1 Coordinate Lymphatic Endothelial Cell Expansion and Contraction during an Inflammatory Immune Response +image: /images/2018-lucas.jpg +date: 'September 15, 2018' + +categories: [project-1, project-2, core-b] +about: + id: about + template: jolla + links: + - text: Publication + icon: file-earmark + href: https://pubmed.ncbi.nlm.nih.gov/30045970/ +--- + +[Erin Lucas](http://orcid.org/0000-0001-7705-2069), Jeffrey Finlon, Matthew Burchill, Mary McCarthy, [Thomas Morrison](https://scholar.google.com/citations?user=ljkm0eMAAAAJ&hl=en&oi=ao), Tonya Colpitts, Beth Tamburini + +Lymph node (LN) expansion during an immune response is a complex process that involves the relaxation of the fibroblastic network, germinal center formation, and lymphatic vessel growth. These processes require the stromal cell network of the LN to act deliberately to accommodate the influx of immune cells to the LN. The molecular drivers of these processes are not well understood. Therefore, we asked whether the immediate cytokines type 1 IFN produced during viral infection influence the lymphatic network of the LN in mice. We found that following an IFN-inducing stimulus such as viral infection or polyI:C, programmed cell death ligand 1 (PD-L1) expression is dynamically upregulated on lymphatic endothelial cells (LECs). We found that reception of type 1 IFN by LECs is important for the upregulation of PD-L1 of mouse and human LECs and the inhibition of LEC expansion in the LN. Expression of PD-L1 by LECs is also important for the regulation of LN expansion and contraction after an IFN-inducing stimulus. We demonstrate a direct role for both type 1 IFN and PD-L1 in inhibiting LEC division and in promoting LEC survival. Together, these data reveal a novel mechanism for the coordination of type 1 IFN and PD-L1 in manipulating LEC expansion and survival during an inflammatory immune response. diff --git a/pubs/2018-mccarthy/index.qmd b/pubs/2018-mccarthy/index.qmd new file mode 100644 index 0000000..da0293e --- /dev/null +++ b/pubs/2018-mccarthy/index.qmd @@ -0,0 +1,18 @@ +--- +title: Chikungunya virus impairs draining lymph node function by inhibiting HEV-mediated lymphocyte recruitment +image: /images/2018-mccarthy.jpg +date: 'July 12, 2018' + +categories: [project-1, project-2, core-b] +about: + id: about + template: jolla + links: + - text: Publication + icon: file-earmark + href: https://pubmed.ncbi.nlm.nih.gov/29997290/ +--- + +Mary McCarthy, Bennett Davenport, Glennys Reynoso, [Erin Lucas](http://orcid.org/0000-0001-7705-2069), Nicholas May, Susan Elmore, Beth Tamburini, Heather Hickman, [Thomas Morrison](https://scholar.google.com/citations?user=ljkm0eMAAAAJ&hl=en&oi=ao) + +Chikungunya virus (CHIKV) causes acute and chronic rheumatologic disease. Pathogenic CHIKV strains persist in joints of immunocompetent mice, while the attenuated CHIKV strain 181/25 is cleared by adaptive immunity. We analyzed the draining lymph node (dLN) to define events in lymphoid tissue that may contribute to CHIKV persistence or clearance. Acute 181/25 infection resulted in dLN enlargement and germinal center (GC) formation, while the dLN of mice infected with pathogenic CHIKV became highly disorganized and depleted of lymphocytes. Using CHIKV strains encoding ovalbumin-specific TCR epitopes, we found that lymphocyte depletion was not due to impaired lymphocyte proliferation. Instead, the accumulation of naive lymphocytes transferred from the vasculature to the dLN was reduced, which was associated with fewer high endothelial venule cells and decreased CCL21 production. Following NP-OVA immunization, NP-specific GC B cells in the dLN were decreased during pathogenic, but not attenuated, CHIKV infection. Our data suggest that pathogenic, persistent strains of CHIKV disable the development of adaptive immune responses within the dLN. diff --git a/pubs/2019-tamburini/index.qmd b/pubs/2019-tamburini/index.qmd new file mode 100644 index 0000000..5513ccd --- /dev/null +++ b/pubs/2019-tamburini/index.qmd @@ -0,0 +1,18 @@ +--- +title: Chronic Liver Disease in Humans Causes Expansion and Differentiation of Liver Lymphatic Endothelial Cells +image: /images/2019-tamburini.jpg +date: 'May 15, 2019' + +categories: [project-2, core-b, core-c, core-d] +about: + id: about + template: jolla + links: + - text: Publication + icon: file-earmark + href: https://pubmed.ncbi.nlm.nih.gov/31156626/ +--- + +Beth Tamburini, Jeffrey Finlon, Austin Gillen, Michael Kriss, Kent Riemondy, Rui Fu, Ronald Schuyler, [Jay Hesselberth](https://scholar.google.com/citations?user=EnOmNEYAAAAJ), Hugo Rosen, Matthew Burchill + +Liver lymphatic vessels support liver function by draining interstitial fluid, cholesterol, fat, and immune cells for surveillance in the liver draining lymph node. Chronic liver disease is associated with increased inflammation and immune cell infiltrate. However, it is currently unknown if or how lymphatic vessels respond to increased inflammation and immune cell infiltrate in the liver during chronic disease. Here we demonstrate that lymphatic vessel abundance increases in patients with chronic liver disease and is associated with areas of fibrosis and immune cell infiltration. Using single-cell mRNA sequencing and multi-spectral immunofluorescence analysis we identified liver lymphatic endothelial cells and found that chronic liver disease results in lymphatic endothelial cells (LECs) that are in active cell cycle with increased expression of CCL21. Additionally, we found that LECs from patients with NASH adopt a transcriptional program associated with increased IL13 signaling. Moreover, we found that oxidized low density lipoprotein, associated with NASH pathogenesis, induced the transcription and protein production of IL13 in LECs both in vitro and in a mouse model. Finally, we show that oxidized low density lipoprotein reduced the transcription of PROX1 and decreased lymphatic stability. Together these data indicate that LECs are active participants in the liver, expanding in an attempt to maintain tissue homeostasis. However, when inflammatory signals, such as oxidized low density lipoprotein are increased, as in NASH, lymphatic function declines and liver homeostasis is impeded. diff --git a/pubs/2020-lucas/index.qmd b/pubs/2020-lucas/index.qmd new file mode 100644 index 0000000..f5b6ad0 --- /dev/null +++ b/pubs/2020-lucas/index.qmd @@ -0,0 +1,18 @@ +--- +title: PD-L1 Reverse Signaling in Dermal Dendritic Cells Promotes Dendritic Cell Migration Required for Skin Immunity +image: /images/2020-lucas.jpg +date: 'October 13, 2020' + +categories: [project-2, core-b] +about: + id: about + template: jolla + links: + - text: Publication + icon: file-earmark + href: https://pubmed.ncbi.nlm.nih.gov/33053342/ +--- + +[Erin Lucas](http://orcid.org/0000-0001-7705-2069), Johnathon Schafer, [Jennifer Matsuda](https://scholar.google.com/citations?user=xNd-F7YAAAAJ), Madison Kraus, Matthew Burchill, Beth Tamburini + +Although the function of the extracellular region of programmed death ligand 1 (PD-L1) through its interactions with PD-1 on T cells is well studied, little is understood regarding the intracellular domain of PD-L1. Here, we outline a major role for PD-L1 intracellular signaling in the control of dendritic cell (DC) migration from the skin to the draining lymph node (dLN). Using a mutant mouse model, we identify a TSS signaling motif within the intracellular domain of PD-L1. The TSS motif proves critical for chemokine-mediated DC migration to the dLN during inflammation. This loss of DC migration, in the PD-L1 TSS mutant, leads to a significant decline in T cell priming when DC trafficking is required for antigen delivery to the dLN. Finally, the TSS motif is required for chemokine receptor signaling downstream of the Gα subunit of the heterotrimeric G protein complex, ERK phosphorylation, and actin polymerization in DCs. diff --git a/pubs/2021-carpentier/2021-carpentier.jpg b/pubs/2021-carpentier/2021-carpentier.jpg deleted file mode 100644 index 7d13bfe..0000000 Binary files a/pubs/2021-carpentier/2021-carpentier.jpg and /dev/null differ diff --git a/pubs/2021-carpentier/index.qmd b/pubs/2021-carpentier/index.qmd index a292006..a123157 100644 --- a/pubs/2021-carpentier/index.qmd +++ b/pubs/2021-carpentier/index.qmd @@ -1,7 +1,9 @@ --- title: MARCO+ lymphatic endothelial cells sequester arthritogenic alphaviruses to limit viremia and viral dissemination -image: 2021-carpentier.jpg -categories: [project-1, project-2, core-c, core-d] +image: /images/2021-carpentier.jpg +date: 'November 15, 2021' + +categories: [project-1, project-2, core-b, core-c, core-d] about: id: about template: jolla diff --git a/pubs/2021-walsh/2021-walsh.jpg b/pubs/2021-walsh/2021-walsh.jpg deleted file mode 100644 index 54d3e97..0000000 Binary files a/pubs/2021-walsh/2021-walsh.jpg and /dev/null differ diff --git a/pubs/2021-walsh/index.qmd b/pubs/2021-walsh/index.qmd index bf4c21e..53c53fd 100644 --- a/pubs/2021-walsh/index.qmd +++ b/pubs/2021-walsh/index.qmd @@ -1,7 +1,9 @@ --- title: Molecular tracking devices quantify antigen distribution and archiving in the murine lymph node -image: 2021-walsh.jpg -categories: [project-2, core-c, core-d] +image: /images/2021-walsh.jpg +date: 'April 12, 2021' + +categories: [project-2, core-b, core-c, core-d] about: id: about template: jolla diff --git a/pubs/2022-doan/2022-doan.jpg b/pubs/2022-doan/2022-doan.jpg deleted file mode 100644 index 3349aa9..0000000 Binary files a/pubs/2022-doan/2022-doan.jpg and /dev/null differ diff --git a/pubs/2022-doan/index.qmd b/pubs/2022-doan/index.qmd index 84df59d..88bbb16 100644 --- a/pubs/2022-doan/index.qmd +++ b/pubs/2022-doan/index.qmd @@ -1,7 +1,9 @@ --- title: Trafficking and retention of protein antigens across systems and immune cell types -image: 2022-doan.jpg -categories: [project-2] +image: /images/2022-doan.jpg +date: 'May 03, 2022' + +categories: [project-2, core-b] about: id: about template: jolla diff --git a/pubs/2023-tamburini/index.qmd b/pubs/2023-tamburini/index.qmd new file mode 100644 index 0000000..6e834ff --- /dev/null +++ b/pubs/2023-tamburini/index.qmd @@ -0,0 +1,18 @@ +--- +title: Vaccine-induced antigen archiving enhances local memory CD8+ T cell responses following an unrelated viral infection +image: /images/2023-tamburini.jpg +date: 'September 25, 2023' + +categories: [project-1, project-2, core-b, core-c, core-d] +about: + id: about + template: jolla + links: + - text: Publication + icon: file-earmark + href: https://pubmed.ncbi.nlm.nih.gov/37841845/ +--- + +Beth Tamburini, Thu Doan, Tadg Forward, [Erin Lucas](http://orcid.org/0000-0001-7705-2069), Ira Fleming, Aspen Uecker-Martin, [Jay Hesselberth](https://scholar.google.com/citations?user=EnOmNEYAAAAJ), [Thomas Morrison](https://scholar.google.com/citations?user=ljkm0eMAAAAJ&hl=en&oi=ao) + +Viral and vaccine antigens persist or are archived in lymph node stromal cells (LNSC) such as lymphatic endothelial cells (LEC) and fibroblastic reticular cells (FRC). Here, we find that, during the time frame of antigen archiving, LEC apoptosis caused by a second, but unrelated, innate immune stimulus such as vaccina viral infection or CpG DNA administration boosted memory CD8+ T cells specific to the archived antigen. In contrast to "bystander" activation associated with unrelated infections, the memory CD8+ T cells specific to the vaccine archived antigen were significantly higher than memory CD8+ T cells of a different antigen specificity. Finally, the boosted memory CD8+ T cells resulted in increased protection against Listeria monocytogenes expressing the vaccine antigen, but only for the duration that the vaccine antigen was archived. These findings outline a novel mechanism by which LNSC archived antigens, in addition to bystander activation, can augment memory CD8+ T cell responses during repeated inflammatory insults. diff --git a/pubs/2024-kim/index.qmd b/pubs/2024-kim/index.qmd new file mode 100644 index 0000000..1b1df6e --- /dev/null +++ b/pubs/2024-kim/index.qmd @@ -0,0 +1,17 @@ +--- +title: Anaerobic respiration of host-derived methionine sulfoxide protects intracellular Salmonella from the phagocyte NADPH oxidase +date: 'January 24, 2024' + +categories: [project-1, core-b] +about: + id: about + template: jolla + links: + - text: Publication + icon: file-earmark + href: https://pubmed.ncbi.nlm.nih.gov/38307020/ +--- + +Ju-Sim Kim, Lin Liu, Sashi Kant, David Orlicky, Siva Uppalapati, Alyssa Margolis, Bennett Davenport, [Thomas Morrison](https://scholar.google.com/citations?user=ljkm0eMAAAAJ&hl=en&oi=ao), [Jennifer Matsuda](https://scholar.google.com/citations?user=xNd-F7YAAAAJ), Michael McClelland, Jessica Jones-Carson, Andres Vazquez-Torres + +Intracellular Salmonella experiencing oxidative stress downregulates aerobic respiration. To maintain cellular energetics during periods of oxidative stress, intracellular Salmonella must utilize terminal electron acceptors of lower energetic value than molecular oxygen. We show here that intracellular Salmonella undergoes anaerobic respiration during adaptation to the respiratory burst of the phagocyte NADPH oxidase in macrophages and in mice. Reactive oxygen species generated by phagocytes oxidize methionine, generating methionine sulfoxide. Anaerobic Salmonella uses the molybdenum cofactor-containing DmsABC enzymatic complex to reduce methionine sulfoxide. The enzymatic activity of the methionine sulfoxide reductase DmsABC helps Salmonella maintain an alkaline cytoplasm that supports the synthesis of the antioxidant hydrogen sulfide via cysteine desulfuration while providing a source of methionine and fostering redox balancing by associated dehydrogenases. Our investigations demonstrate that nontyphoidal Salmonella responding to oxidative stress exploits the anaerobic metabolism associated with dmsABC gene products, a pathway that has accrued inactivating mutations in human-adapted typhoidal serovars. diff --git a/pubs/2024-lucas/index.qmd b/pubs/2024-lucas/index.qmd index 4cf46a2..838a7b0 100644 --- a/pubs/2024-lucas/index.qmd +++ b/pubs/2024-lucas/index.qmd @@ -1,6 +1,8 @@ --- title: Chikungunya virus infection disrupts lymph node lymphatic endothelial cell composition and function via MARCO -categories: [project-1, project-2, core-c, core-d] +date: 'January 09, 2024' + +categories: [project-1, project-2, core-b, core-c, core-d] about: id: about template: jolla