Inhibition of interleukin 2 by serum in healthy individuals and in patients with autoimmune disease.
To study the mechanisms that regulate the activity of interleukin 2 (IL 2) and possibly limit its activity, we have examined normal human serum for its ability to inhibit IL 2-mediated proliferation of a cloned IL 2-dependent cytotoxic T lymphocyte line (CTLL). Normal human serum contains a factor capable of inhibiting IL 2 dependent proliferation of CTLL cells. This factor is absorbed with the cells but not IL 2 molecules. The inhibitor is heat-labile and inactivated by trypsin treatment. The molecular weight of the inhibitor is 70,000-220,000. The imbalance of the inhibitor is observed in serum from patients with autoimmune disease including systemic lupus erythematosus and rheumatoid arthritis. These results suggest that the serum IL 2 inhibitor may play an important role in the in vivo regulatory mechanism of IL 2 activity and in aberrant immune functions in humans.
D001172:Arthritis, Rheumatoid / Q000097:blood*; D001327:Autoimmune Diseases / Q000097:blood*; D006801:Humans; D007376:Interleukin-2 / Q000037:antagonists & inhibitors*; D008180:Lupus Erythematosus, Systemic / Q000097:blood*; D008213:Lymphocyte Activation / Q000187:drug effects; D008222:Lymphokines / Q000097:blood* / Q000494:pharmacology; D008970:Molecular Weight; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects
D007376:Interleukin-2; D008222:Lymphokines; C046147:interleukin 2 inhibitor