Abstract
Abstract Endogenous mammary tumor virus (Mtv29)-encoded superantigen (vSAg29) mediates “reverse immune surveillance” that characterizes SJL lymphoma (RCS) development. CD4+Vβ16+ vSAg29-responsive T cells provide growth factors (notably IL-5 and IL-4) for RCS growth. The vSAg29-responsive CD4+ T cells belong to both CD4+CD25+ (Treg) and CD4+CD25− (non-Treg) populations. Unlike the known inhibitory ability of Treg cell on non-Treg cell responses to nominal antigens, Treg cells responding to vSAg29 fail to inhibit response of vSAg29-responsive non-Treg cells. This unique behavior of vSAg29-responsive T cells was found to be linked to their differential expression of cytokine, chemokine and toll-like receptor family genes. Treg cells responding to vSAg29 significantly inhibited the production of IL-4, IL-5, IL-10, IFN-γ, CCR4, CCL17, TOLLIP, UBE2N, NFKBIB, by CD4+CD25− cells. On the other hand, the addition of CD4+ Treg cells to non-Treg cells responding to vSAg29, resulted in enhanced production of mRNA for MIF, IL-10R, BCL6, CXCL4 (PF4), MAPK8 (JNK1), UBE2V1. Research funded by CA10273 from NCI.
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