Fas ligand expression and function in systemic lupus erythematosus.

摘要: Mutations in the Fas receptor or its ligand (FasL) lead to lupus-like systemic autoimmune diseases mice and some humans. To determine whether a significant number of patients with lupus erythematosus (SLE) have impaired FasL function, we compared T cell effector function by superantigen-activated CD4+ lines anti-CD3- IL-2-generated cytotoxic cells. No differences were observed between SLE normal control superantigen-derived cells either ability these up-regulate expression induce apoptosis Fas-sensitive target B When anti-CD3/IL-2-activated examined, had modest reduction (-8%) cytotoxicity controls, but was similar rheumatoid arthritis disease controls. A evident both perforin/granzyme pathways as determined testing Fas-positive -negative targets well selective blockade pathway concanamycin. These results indicate that no specific defects are majority under vitro conditions tested. The proportional following anti-CD3/IL-2 stimulation most likely reflects subtle activation patient-derived vs