Effects of anti-CD2 antibodies on CD4+ T cells programmed to apoptosis.
Int Conf AIDS 1996 Jul 7-12; 11:4 (abstract no. We.A.105) Gilardini M, Piazza C, Cundari E, Moretti S, Tuosto L, Acuto O, Piccolella E; Dept. of Cellular and Developmental Biology, University of Rome "La Sapienza", Rome, Italy. Fax: (39-6) 499-17594.
It is well established that a temporal or absolute imbalance of signals delivered via T cell antigen receptor (TcR) and the CD4 co-receptor can lead to anergy and/or apoptosis. It has also been reported that the interaction of the accessory molecule CD2 with its ligand LFA-3, is able to provide signals that protect T cells from the induction of anergy. Moreover our data have evidenced that T cell clones programmed to apoptosis by gp120 or anti-CD4 antibodies, before TcR ligation, were rescued by the interaction with antigen presenting cells expressing LFA-3 molecules and this appeared to be the result of augmented interleukin-2 (IL-2) and IL-4 release. However, neither LFA-3 nor IL-2 and IL-4 were able to reconstitute T cell proliferation, maintaining T cells in a non-responsive state. To investigate this phenomenon, using anti-CD2 antibodies, we analyzed both the CD2-mediated transduction signals and the IL-2 receptor expression. Our results clearly demonstrate that CD2 engagement, mediated by anti-CD2 antibodies, provides T cells with both survival and proliferative signals. The analysis of the levels of protein phosphorilation of CD4+ T cells treated with agonistic antibodies to TcR or CD2 suggests that CD2 engagement might activate a transduction pathway alternative to that provided by TcR. Concluding, it is interesting to evaluate the possibility to use anti-CD2 antibodies as a new therapeutic approach to block immunosuppression and apoptotic events partcularly during the early stages of HIV disease.
Keywords: AEGIS, Antigens, CD2, Antigens, CD4, T-Lymphocytes, Apoptosis, Receptors, Antigen, T-Cell, Antigens, CD58, Interleukin-2, Antibodies, Anti-Idiotypic, Interleukin-4, Antigen-Presenting Cells, Receptors, Interleukin-2, Immune Tolerance, immunology, ICA11
