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PMID:9368605
Citation |
Zhou, Q, Wu, Y, Nielsen, PJ and Liu, Y (1997) Homotypic interaction of the heat-stable antigen is not responsible for its co-stimulatory activity for T cell clonal expansion. Eur. J. Immunol. 27:2524-8 |
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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. |
Links |
PubMed Online version:10.1002/eji.1830271009 |
Keywords |
Animals; Antigens, CD/genetics; Antigens, CD/immunology; Antigens, CD24; CD4-Positive T-Lymphocytes/immunology; CHO Cells; Cell Division; Cricetinae; Flow Cytometry; Lymphocyte Activation/physiology; Membrane Glycoproteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Receptor-CD3 Complex, Antigen, T-Cell/immunology; Recombinant Fusion Proteins/biosynthesis; Recombinant Fusion Proteins/immunology |
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Significance
Annotations
Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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