期刊
IMMUNOLOGY AND CELL BIOLOGY
卷 90, 期 8, 页码 784-795出版社
WILEY
DOI: 10.1038/icb.2012.1
关键词
contact sensitivity; epicutaneous immunization; Tc1 lymphocytes; Treg cells
资金
- Ministry of Science and Higher Education [N N401 006939, N N401 545940, N N401 000936, JDRF 1-2007-586]
- NIDDK [RC1DK08769, DERC]
As we have shown previously that protein antigen applied epicutaneously (EC) in mice inhibits TNP-specific Th1-mediated contact sensitivity (CS), we postulated that the maneuver of EC immunization might also suppress Tc1-dependent CS response. Here we showed that EC immunization of normal mice with 2,4-dinitrophenylated bovine serum albumin (DNP-BSA) applied on the skin in the form of a patch induces a state of subsequent unresponsiveness due to regulatory T cells (Treg) that inhibited sensitization and elicitation of effector T-cell responses. Suppression is transferable in vivo by TCR alpha beta(+) CD4(+) CD25(+) lymphocytes harvested from lymph nodes (LNs) of skin-patched animals. Flow cytometry revealed that EC immunization with DNP-BSA increased TCR alpha beta(+) CD4(+) CD25(+) FoxP3(+) lymphocytes in subcutaneous LNs, suggesting that observed suppression was mediated by Treg cells. Further, in vitro experiments showed that EC immunization with DNP-BSA prior to 1-fluoro-2,4-dinitrobenzen sensitization suppressed LN cell proliferation and inhibited production of TNF-alpha, IL-12 and IFN-gamma. Using a transwell system or anti-CTLA-4 mAb, we found that EC induced suppression required direct Treg-effector cell contact and is CTLA-4-dependent. Immunology and Cell Biology (2012) 90, 784-795; doi:10.1038/icb.2012.1; published online 31 January 2012
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