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Regulatory T cells and superantigen‐induced toxic shock. A study using HLA class II transgenic mice
Author(s) -
Rajagopalan Govindarajan,
Epstein Benjamin,
Lytle Anna,
David Chella
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.848.11
Subject(s) - superantigen , foxp3 , il 2 receptor , microbiology and biotechnology , biology , immunology , elispot , flow cytometry , enterotoxin , andrology , cd8 , t cell , antigen , immune system , medicine , gene , biochemistry , escherichia coli
To understand the role of regulatory T cells in staphylococcal enterotoxin B‐induced toxic shock syndrome (TSS), we performed gene expression profiling in HLA‐DR3 transgenic mice using microarrays. We observed that at 3 hours after systemic exposure to SEB (10 μg), the splenic expression of FoxP3, a hall mark of regulatory T cells, was increased by 5 folds (p<0.005). In addition, other genes that regulate FoxP3 + Tregs were also significantly modulated by SEB. These include IL‐2R (27‐fold), IL‐2 (234‐fold), IL‐6 (689‐fold), IL‐21 (21‐fold), TGF‐B1 (0.7‐fold), IL‐17 (5.5‐fold) and IL‐22 (98‐fold). To further characterize the homeostasis of Tregs cells during superantigen‐induced TSS in vivo, HLA‐DR3 transgenic mice were first challenged with SEB and were administered BrdU in drinking water for 3 days. Mice were killed 3 days later and splenocytes analyzed by flow cytometry. We observed that in addition to FoxP3‐TCR Vβ8 + T cells, FoxP3 + TCR Vβ8 + T cells also significantly expanded in vivo as evident from their BrdU staining patterns. This indicated that SEB is able to activate Tregs as well. Depletion of Tregs using anti‐CD25 antibodies (clone PC‐61, 500 ug/mouse) 2 days prior to SEB challenge did not significantly alter serum cytokine levels as compared to control mice treated with rat IgG and SEB. Thus, T regulatory cells have a minimal role in SEB‐induced TSS.