Impaired mobility of human T lymphocyte surface molecules during inactive systemic lupus erythematosus. Relationship to a defective cAMP pathway

Abstract

The T lymphocytes of patients with active systemic lupus erythematosus (SLE) exhibit impaired capping of the surface molecules CD3, CD4, and CD8 and a defective cAMP-dependent pathway. Since the mobility of these molecules is regulated in part by cAMP, we sought to determine whether there is a specific defect(s) along the T cell cAMP pathway that contributes to the persistent capping disorder observed during inactive SLE. The data suggest that a defect may exist at the level of cAMP-dependent protein kinase activation or at a point distally. We propose that a disorder of cAMP-dependent protein kinase activity might account for the defect of capping observed in both the CD3, CD4 (helper/inducer) and CD3, CD8 (suppressor) subsets observed in SLE.