Responsiveness of systemic lupus erythematosus T cells to signals provided through LCA T200 (CD45) and T1 (CD5) antigens.

It is currently unclear whether the T cell defective capacity to proliferate and to secrete interleukin-2 (IL-2) observed in systemic lupus erythematosus (SLE) reflects an intrinsic disorder of the T cell or defects secondary to a monocyte dysfunction. In order to clarify whether the disorder is intrinsic to the T cell, we have studied the proliferative capacity of cells highly depleted of monocytes, activated by Seph-CD3, as 'first signal,' and by monoclonal antibodies (MoAbs) CD45 and CD5 as 'second signal,' in 14 SLE patients. There were no significant differences between SLE patients and healthy volunteers in the response of the monocyte-depleted cells to Seph-CD3+CD45; Seph-CD3+CD5; Seph-CD3+IL-2; and Seph-CD3+phorbol myristate acetate (PMA). However, active SLE compared with non-active SLE had an impaired response of peripheral blood mononuclear cells (PBMC) to Seph-CD3 and to Seph-CD3+IL-2. The good responses obtained to second signals provided through CD45 and CD5 indicate that at least these mechanisms are not intrinsically impaired in SLE T cells. These findings, together with the abnormal response of PBMC suggest that a monocyte dysfunction plays an important role in SLE T cells hyporesponsiveness.