Homotypic interaction of the heat‐stable antigen is not responsible for its co‐stimulatory activity for T cell clonal expansion

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Abstract
The heat‐stable antigen (HSA) is an important co‐stimulatory molecule on antigen‐presenting cells (APC). However, the receptor on T cells that receives the co‐stimulatory signal from HSA has not been identified. Because the HSA is transiently expressed on T cells after the T cell receptor/CD3 complex is engaged, and because it can bind to itself in a homotypic fashion, it has been proposed that homotypic interaction of HSA is responsible for its co‐stimulatory activity. Here we test this hypothesis using mice that have a targeted mutation of the HSA gene, as well as novel transgenic mice that constitutively express HSA on T cells. We show that HSA‐deficient T cells remain responsive to co‐stimulation by HSA. Furthermore, constitutive expression of HSA does not enhance T cell response to co‐stimulatory by HSA. Taken together, our results demonstrate that homotypic interaction of HSA is not responsible for co‐stimulation mediated by HSA expressed on APC.