Homotypic interaction of the heat-stable antigen is not responsible for its co-stimulatory activity for T cell clonal expansion.
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.
Zhou
Q
Q
Michael Heidelberger Division of Immunology, Department of Pathology, New York University Medical Center, New York 10016, USA.
Wu
Y
Y
Nielsen
P J
PJ
Liu
Y
Y
D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000276:immunology*; D051927:CD24 Antigen; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D016466:CHO Cells; D002455:Cell Division; D006224:Cricetinae; D005434:Flow Cytometry; D008213:Lymphocyte Activation / Q000502:physiology*; D008562:Membrane Glycoproteins; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D017260:Receptor-CD3 Complex, Antigen, T-Cell / Q000276:immunology*; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis / Q000276:immunology
D015703:Antigens, CD; D051927:CD24 Antigen; C497890:Cd24a protein, mouse; D008562:Membrane Glycoproteins; D017260:Receptor-CD3 Complex, Antigen, T-Cell; D011993:Recombinant Fusion Proteins