Regulatory T Cells Modulate Staphylococcal Enterotoxin B-Induced Effector T-Cell Activation and Acceleration of Colitis

Department of Medicine, Division of Gastroenterology, Mount Sinai Hospital, and Medical Sciences Division, University of Toronto, Canada.
Infection and immunity (Impact Factor: 3.73). 02/2009; 77(2):707-13. DOI: 10.1128/IAI.00822-08
Source: PubMed


Oral administration of bacterial superantigen Staphylococcus aureus enterotoxin B (SEB) activates mucosal T cells but does not cause mucosal inflammation. We examined the effect of oral SEB
on the development of mucosal inflammation in mice in the absence of regulatory T (Treg) cells. SCID mice were fed SEB 3 and
7 days after reconstitution with CD4+ CD45RBhigh or CD4+ CD45RBhigh plus CD4+ CD45RBlow T cells. Mice were sacrificed at different time points to examine changes in tissue damage and in T-cell phenotypes. Feeding
SEB failed to produce any clinical effect on SCID mice reconstituted with CD4+ CD45RBhigh and CD4+ CD45RBlow T cells, but feeding SEB accelerated the development of colitis in SCID mice reconstituted with CD4+ CD45RBhigh T cells alone. The latter was associated with an increase in the number of CD4+ Vβ8+ T cells expressing CD69 and a significantly lower number of CD4+ CD25+ Foxp3+ T cells. These changes were not observed in SCID mice reconstituted with both CD45RBhigh and CD45RBlow T cells. In addition, SEB impaired the development of Treg cells in the SCID mice reconstituted with CD4+ CD45RBhigh T cells alone but had no direct effect on Treg cells. In the absence of Treg cells, feeding SEB induced activation of mucosal
T cells and accelerated the development of colitis. This suggests that Treg cells prevent SEB-induced mucosal inflammation
through modulation of SEB-induced T-cell activation.

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Available from: Cathy Streutker, Jan 08, 2014
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