Stimulation of the beta-subunit of the IL-2 receptor induces MHC-unrestricted cytotoxicity in T acute lymphoblastic leukemia cells and normal thymocytes.
Recently, several laboratories have identified a novel protein(s) of 70,000 to 75,000 Da (IL-2R beta-subunit) that, when expressed with the p55 Tac protein (alpha-subunit), imparts high affinity IL-2 binding. Expression of the beta-subunit mediates acquisition of MHC-unrestricted cytotoxicity in large granular lymphocytes. We report that thymocytes and T acute lymphoblastic leukemia cells express the beta-subunit of the IL-2R in the absence of detectable alpha-subunit expression and that IL-2 induces acquisition of MHC-unrestricted cytotoxic activity in these cells through stimulation of the beta-subunit.
D002648:Child; D003602:Cytotoxicity, Immunologic; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism; D007945:Leukemia, Lymphoid / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D008285:Major Histocompatibility Complex; D010641:Phenotype; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000378:metabolism; D011971:Receptors, Immunologic / Q000302:isolation & purification / Q000378:metabolism*; D015375:Receptors, Interleukin-2; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D013950:Thymus Gland / Q000166:cytology* / Q000378:metabolism
D007376:Interleukin-2; D011948:Receptors, Antigen, T-Cell; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2