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Involvement of "accessory" and antigen receptor molecules in human helper T cell clone activation studied by
G Pawelec1, A Rehbein, I Balko
1Immunology Laboratory, Medizinische Klinik, Tübingen, Federal Republic of Germany.
The requirements for activation of autocrine proliferation in human helper T cell clones (Th-TCC) by allogeneic cells were examined in monoclonal antibody (MoAb) blocking studies. Stimulation was not blocked by CD4, CD5, CD6, CD7, or CD45 MoAbs, despite high levels of expression of these antigens on the TCC. Only CD2 and CD11a (LFA-1) MoAbs blocked activation, the latter only when peripheral blood mononuclear cells (PBMCs) and not B-lymphoblastoid cell line (B-LCL) cells were used at stimulators. Responses to interleukin 2 (IL 2) were only minimally blocked by any of the MoAbs. All TCC were CD3+ and expressed the alpha/beta chain T cell receptor (TCR) as detected by moAb WT31. Accordingly, CD3 and WT31 MoAbs consistently blocked stimulation by B-LCL, and in addition one anti-DR5 TCC and one anti-DQw3 TCC were blocked by MoAb 42/1C1, which is directed to an idiotypic determinant of the HPB-ALL leukemic line TCR. Only these two TCC reacted with moAb 42/1C1 in flow cytometry. These observations suggest that CD2- but not LFA-1-mediated interactions, as well as TCR and stimulating antigen binding, are absolutely necessary to activate Th-TCC.
The requirements for activation of autocrine proliferation in human helper T cell clones (Th-TCC) by allogeneic cells were examined in monoclonal antibody (MoAb) blocking studies. Stimulation was not blocked by CD4, CD5, CD6, CD7, or CD45 MoAbs, despite high levels of expression of these antigens on the TCC. Only CD2 and CD11a (LFA-1) MoAbs blocked activation, the latter only when peripheral blood mononuclear cells (PBMCs) and not B-lymphoblastoid cell line (B-LCL) cells were used at stimulators. Responses to interleukin 2 (IL 2) were only minimally blocked by any of the MoAbs. All TCC were CD3+ and expressed the alpha/beta chain T cell receptor (TCR) as detected by moAb WT31. Accordingly, CD3 and WT31 MoAbs consistently blocked stimulation by B-LCL, and in addition one anti-DR5 TCC and one anti-DQw3 TCC were blocked by MoAb 42/1C1, which is directed to an idiotypic determinant of the HPB-ALL leukemic line TCR. Only these two TCC reacted with moAb 42/1C1 in flow cytometry. These observations suggest that CD2- but not LFA-1-mediated interactions, as well as TCR and stimulating antigen binding, are absolutely necessary to activate Th-TCC.