Simultaneous cross-linking of CD6 and CD28 induces cell proliferation in resting T cells.

摘要: In the present study, we showed that simultaneous ligation of monoclonal antibodies (mAb) against CD6 and CD28 induces T-cell proliferation in purified resting T lymphocytes absence receptor (TCR) occupancy. No cell was observed when mAb were cross-linked alone or used simultaneously soluble form. mediated through CD6/CD28 is accompanied by up-regulation interleukin-2 (IL-2) mRNA expression IL-2 receptors on surface. presence IL-2-neutralizing proliferative response induced inhibited dose dependently. Cross-linking to together did not down-regulate CD3/TCR complex. only partially blocked immunosuppressive drug, cyclosporin A (CsA), whereas anti-CD28-induced phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), unaffected. sharp contrast anti-CD6 TPA efficiently CsA. addition, two protein kinase C (PKC) inhibitors, GF 109203X H-7 dose-dependently CD6/CD28, suggesting PKC activation may be involved. Furthermore, there a marked differential dose-dependent inhibitory effect inhibitors co-ligation anti-CD28 anti-CD3, with former being more sensitive inhibition. Taken collectively, our results suggest can occur an antigen-independent pathway cross-linking accessory molecules, CD28, these surface antigens have distinct signalling pathways.