Class II MHC Deficient Mice Have Contact Hypersensitivity Responses that Are Regulated by CD4+CD25+ T Cells (88.5)

CD4+CD25+ T cells limit the expansion of effector CD8 T cells in skin draining lymph nodes (LN) during hapten sensitization for contact hypersensitivity (CHS) responses. This regulatory function results in decreased swelling responses to hapten challenge of the skin. Depletion of CD4 T cells prior to hapten sensitization results in increased numbers of hapten-primed effector CD8 T cells and CHS responses that are elevated in magnitude and extended in duration. These increased CHS responses are similar to those observed in sensitized and challenged class II MHC−/− mice. However, depletion of CD4 T cells in class II MHC−/− mice increased CHS responses to hapten sensitization and challenge when compared to untreated class II MHC−/− mice. ELISPOT analyses indicated increased hapten-specific CD8 T cell priming in LN of class II MHC−/− mice compared to the wild-type and these numbers increased significantly with anti-CD4 or anti-CD25 mAb treatment prior to sensitization. Flow cytometry analyses of LN cells from class II MHC−/− mice revealed a small but distinct population of CD4T cells and ≥50% expressed CD25. qRT-PCR analyses of RNA prepared from LN cells of class II MHC−/− and wild-type mice indicated the presence of FoxP3 expression that was absent when the animals were depleted of CD4 or CD25, but not NK1.1, cells. Purified CD4+ CD25+ T cells from class II MHC−/− and wild-type mice were equivalent in the ability to limit CD4+CD25− T cell proliferation in vitro. These results identify a CD4+ CD25+ regulatory T cell population in class II MHC−/− mice.