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Segmented filamentous bacteria-induced epithelial MHCII regulates cognate CD4<SUP>+</SUP> IELs and epithelial turnover

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F23%3A00578338" target="_blank" >RIV/67985904:_____/23:00578338 - isvavai.cz</a>

  • Alternative codes found

    RIV/61388971:_____/23:00578338 RIV/68378050:_____/23:00578338

  • Result on the web

    <a href="https://rupress.org/jem/article-abstract/221/1/e20230194/276366/Segmented-filamentous-bacteria-induced-epithelial?redirectedFrom=fulltext" target="_blank" >https://rupress.org/jem/article-abstract/221/1/e20230194/276366/Segmented-filamentous-bacteria-induced-epithelial?redirectedFrom=fulltext</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1084/jem.20230194" target="_blank" >10.1084/jem.20230194</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Segmented filamentous bacteria-induced epithelial MHCII regulates cognate CD4<SUP>+</SUP> IELs and epithelial turnover

  • Original language description

    Intestinal epithelial cells have the capacity to upregulate MHCII molecules in response to certain epithelial-adhesive microbes, such as segmented filamentous bacteria (SFB). However, the mechanism regulating MHCII expression as well as the impact of epithelial MHCII-mediated antigen presentation on T cell responses targeting those microbes remains elusive. Here, we identify the cellular network that regulates MHCII expression on the intestinal epithelium in response to SFB. Since MHCII on the intestinal epithelium is dispensable for SFB-induced Th17 response, we explored other CD4(+ )T cell-based responses induced by SFB. We found that SFB drive the conversion of cognate CD4(+) T cells to granzyme(+) CD8 alpha(+) intraepithelial lymphocytes. These cells accumulate in small intestinal intraepithelial space in response to SFB. Yet, their accumulation is abrogated by the ablation of MHCII on the intestinal epithelium. Finally, we show that this mechanism is indispensable for the SFB-driven increase in the turnover of epithelial cells in the ileum. This study identifies a previously uncharacterized immune response to SFB, which is dependent on the epithelial MHCII function.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10606 - Microbiology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2023

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Journal of Experimental Medicine

  • ISSN

    0022-1007

  • e-ISSN

    1540-9538

  • Volume of the periodical

    221

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    26

  • Pages from-to

    e20230194

  • UT code for WoS article

    001096469700001

  • EID of the result in the Scopus database

    2-s2.0-85175500601