Enteroantigen-presenting B cells efficiently stimulate CD4(+) T cells in vitro

Esben Gjerløff Wedebye Schmidt, Nanna Ny Kristensen, Mogens Helweg Claesson, Anders Elm Pedersen

7 Citationer (Scopus)

Abstract

Background: Presentation of enterobacterial antigens by antigen-presenting cells and activation of enteroantigen-specific CD4+ T cells are considered crucial steps in inflammatory bowel disease (IBD) pathology. The detrimental effects of such CD4+ T cells have been thoroughly demonstrated in models of colitis. Also, we have previously established an in vitro assay where murine enteroantigen-specific colitogenic CD4 +CD25- T cells are activated by splenocytes pulsed with an enterobacterial extract. Methods: CD4+CD25- T cells were stimulated in vitro with various kinds of enterobacterial extract-pulsed antigen-presenting cells. T-helper phenotypes were detected by flow cytometry. Results: We found that enteroantigen-pulsed splenic B cells possess a significantly higher and more sustained T cell stimulatory capacity than similarly pulsed splenic dendritic cells (DCs) measured by the level of enteroantigen-specific CD4+CD25- T cell proliferation. In support of this, we observed upregulation of classic maturation markers in B cells following incubation with enterobacterial antigens. Peritoneal and mesenteric lymph node-derived B cells were equally effective as enteroantigen-presenting stimulator cells. B cells greatly expanded the number of stimulated CD4+ T cells, which acquired a TH2 phenotype. Interestingly, regulatory T cells were primarily activated by enteroantigen-pulsed B cells but not by similarly pulsed DCs. Conclusions: We conclude that B cells are superior stimulators of enteroantigen-specific CD4+ T cells in vitro, favoring TH2 polarization. Thus, enteroantigen-processing and -presentation by B cells instead of by DCs might have opposing consequences for IBD development.

OriginalsprogEngelsk
TidsskriftInflammatory Bowel Diseases
Vol/bind17
Udgave nummer1
Sider (fra-til)308-18
Antal sider11
ISSN1078-0998
DOI
StatusUdgivet - jan. 2011

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