endogenous or transgene driven expression of pd l1 on antigenpresenting dcs leads to diminished t cell reactivity in vitro and in vivo as demonstrated in murine models of autoimmunity the importance of pd l1 in self tolerance has also been demonstrated in experimental animals in which blockade or absence of the pd l1 pd 1 pathway results in various forms of autoimmune disease including a spontaneous lupus like glomerulonephritis in c57bl 6 mice the receptor for pd l1 is shared by a second ligand pd l2 b7 dc cd273 which can also inhibit t cell activation but is less widely expressed and appears to play some non redundant roles in self tolerance dna polymorphisms in the gene for the shared pd 1 receptor have been linked to sle susceptibility in some populations of adults and children however t cell expression of pd 1 protein has not been found to differ significantly between sle patients and controls in contrast to the pd 1 gene studies genetic polymorphisms in pd l1 did not appear to be linked to sle however both immature mdc and mo from children with sle failed to up regulate pd l1 normally and this deficiency was associated with increased disease activity indicating an important role for this negative co stimulator in the pathogenesis of sle as discussed above pd l1 on antigen presenting cells binds to pd 1 on t lymphocytes and regulates their activity animals without pd 1 develop an autoimmune disease similar to sle with t lymphocytes reacting to self proteins.