title: I-E expression does not by itself influence growth of or T cell unresponsiveness to SJL lymphomas.
abstract: The nature of the antigen on SJL lymphoma (reticulum cell sarcomas, RCS) cells that is strongly stimulatory to syngeneic CD4+ T cells is still elusive. Previously, we showed that the response to RCS of T cells from F1 hybrids of SJL by strains expressing I-Ak,d and/or I-Ek,d was much lower than that of T cells from SJL mice or from F1 hybrids of SJL by H2b- or H2s-bearing strains. We now show that removal of CD8+T cells from the responding cell population of (SJL x BALB/c)F1 or (SJL x A.TL)F1 mice does not enhance their responses, suggesting that the negative effect of H2k,d is not due to suppressor cells. Moreover, repeated injections of RCS cells into such F1 mice also fail to enhance the response, suggesting that these mice lack responder cells. T cells from I-E alpha transgenic (C57BL x SJL)F1 mice backcrossed to SJL respond to RCS as do T cells from I-E alpha- littermates or SJL mice. Similarly, I-E alpha+ SJL mice support RCS growth in vivo to the same (LN + spleen)/body weight ratio as do I-E- littermates. Thus, while I-E appears to have a negative influence on T cell responsiveness and RCS growth in F1 mice, it does not have such an effect when present, by itself, on a SJL background. The role of V beta 17 a+ T cells in the response of SJL T cells to RCS was also examined, because such cells are known to be responsive to I-E. The responses of V beta 17a(+)-depleted (0.3% V beta 17 a+) and V beta 17 a(+)-enriched (25.3% V beta 17a+) SJL T cell populations to RCS were examined by limiting dilution. We found the incidence of responding cells to be slightly higher in the depleted (0.016%) than in the (0.006%) enriched population. Furthermore, lymph node blast cell populations responding to RCS do not exhibit a higher percentage of cells staining for V beta 17a than do blast cells responding to Con A or unstimulated lymph node cells.
authors.affiliation: Department of Pathology, New York University School of Medicine, New York 10016.
authors.forename: V K
authors.initials: VK
authors.lastname: Tsiagbe
authors.forename: J L
authors.initials: JL
authors.lastname: Rabinowitz
authors.forename: G J
authors.initials: GJ
authors.lastname: Thorbecke
mesh_terms: D000818:Animals; D000949:Histocompatibility Antigens Class II / Q000276:immunology*; D007108:Immune Tolerance; D008213:Lymphocyte Activation; D016403:Lymphoma, Large B-Cell, Diffuse / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D008822:Mice, Transgenic; D011948:Receptors, Antigen, T-Cell / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta; D013601:T-Lymphocytes / Q000276:immunology*; D014407:Tumor Cells, Cultured
chemical_list: D000949:Histocompatibility Antigens Class II; C024138:I-E-antigen; D011948:Receptors, Antigen, T-Cell; D016693:Receptors, Antigen, T-Cell, alpha-beta