Abstract
Abstract CD1d is an antigen presenting molecule structurally similar to MHC class I and presents lipid antigens to natural killer T (NKT) cells. We have previously shown that the mitogen-activated protein kinases (MAPK), p38 and ERK1/2, reciprocally regulate CD1d-mediated antigen presentation--p38 activation leads to its inhibition, whereas ERK1/2 activation leads to its promotion. Transforming growth factor β (TGF β) is a strong regulator of immune responses as well as cell proliferation, apoptosis and differentiation, and can induce the activation of p38. Our studies have shown that CD1d-mediated antigen presentation is inhibited by TGF β in murine LMTK fibroblasts expressing CD1d. Similar inhibition occurs after TGF β treatment of bone marrow-derived dendritic cells (BMDC). Our studies are aimed at dissecting the mechanisms by which TGF β influences CD1d-mediated antigen presentation. This work was supported by NIH grant PO1 AI056097 to RRB.
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