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Regulatory function of CD4+CD25+ T cells from Class II MHC‐deficient mice in contact hypersensitivity responses
Author(s) -
Kish Danielle D.,
Gorbachev Anton V.,
Fairchild Robert L.
Publication year - 2007
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0207089
Subject(s) - il 2 receptor , priming (agriculture) , biology , cd8 , cytotoxic t cell , t cell , mhc class ii , immunology , mhc class i , regulatory t cell , major histocompatibility complex , microbiology and biotechnology , immune system , in vitro , biochemistry , botany , germination
Contact hypersensitivity (CHS) is a CD8+ T cell‐mediated, inflammatory response to hapten sensitization and challenge of the skin. During sensitization, the magnitude and duration of hapten‐specific CD8+ T cell expansion in the skin‐draining lymph nodes (LN) are restricted by CD4+CD25+ T regulatory cells (Treg). The regulation of hapten‐specific CD8+ T cell priming in Class II MHC‐deficient (MHC–/–) mice was investigated. Although hapten‐specific CD8+ T cell priming and CHS responses were elevated in Class II MHC–/– versus wild‐type mice, presensitization depletion of CD4+ or CD25+ cells in Class II MHC–/– mice further increased CD8+ T cell priming and the elicited CHS response. Flow cytometry analyses of LN cells from Class II MHC–/– mice revealed a population of CD4+ T cells with a majority expressing CD25. Forkhead box p3 mRNA was expressed in LN cells from Class II MHC–/– and was reduced to background levels by depletion of CD4+ or CD25+ cells. Isolated CD4+CD25+ T cells from wild‐type and Class II MHC–/– mice limited in vitro proliferation of alloantigen‐ and hapten‐specific T cells to antigen‐presenting stimulator cells. These results identify functional CD4+CD25+ Treg in Class II MHC–/– mice, which restrict hapten‐specific CD8+ T cell priming and the magnitude of CHS responses.