We have further characterized the in vitro phenotype and function of anergic and suppressive CD4(+)25(+) T cells. Following TCR ligation, DO.11.10 CD4(+)25(+) T cells suppress the activation of OT-1 CD8(+)25(-) T cells in an antigen nonspecific manner. Although suppression was seen when using a mixt
Enteroantigen-presenting B cells efficiently stimulate CD4+ T cells in vitro
✍ Scribed by Esben Gjerløff Wedebye Schmidt; Nanna Ny Kristensen; Mogens Helweg Claesson; Anders Elm Pedersen
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 766 KB
- Volume
- 17
- Category
- Article
- ISSN
- 1078-0998
No coin nor oath required. For personal study only.
✦ Synopsis
Background: Presentation of enterobacterial antigens by antigen-presenting cells and activation of enteroantigen-specific CD4 þ T cells are considered crucial steps in inflammatory bowel disease (IBD) pathology. The detrimental effects of such CD4 þ 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 þ CD25 À T cells are activated by splenocytes pulsed with an enterobacterial extract.
Methods: CD4 þ CD25 À 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 þ CD25 À 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 þ T cells, which acquired a T H 2 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 þ T cells in vitro, favoring T H 2 polarization. Thus, enteroantigen-processing and -presentation by B cells instead of by DCs might have opposing consequences for IBD development.
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