Altered regulation of IL-2 production in systemic lupus erythematosus: an evolving paradigm.
In systemic lupus erythematosus (SLE), IL-2 production by T lymphocytes in vitro is impaired. Deficient IL-2 production may be an outcome of a primary SLE T cell disorder that is due to impaired signal transduction. In this issue of the JCI, evidence is presented that an anti-TCR/CD3 complex autoantibody present in SLE sera can bind to T cells and activate the Ca(2+)-calmodulin kinase IV (CaMKIV) signaling cascade, resulting in downregulation of IL-2 transcription and IL-2 production. Because IL-2 may contribute to the maintenance of T cell tolerance, deficient IL-2 production could promote a breach of T cell tolerance that results in autoantibody production in SLE.
Kammer
Gary M
GM
Arthritis Associates Inc., Willoughby, Ohio 44094, USA. gmkammer@hotmail.com
D001323:Autoantibodies / Q000097:blood; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism; D006801:Humans; D007108:Immune Tolerance; D007376:Interleukin-2 / Q000096:biosynthesis*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology*; D017260:Receptor-CD3 Complex, Antigen, T-Cell / Q000276:immunology; D015398:Signal Transduction / Q000502:physiology*; D016176:T-Lymphocyte Subsets; D013601:T-Lymphocytes / Q000378:metabolism*
D001323:Autoantibodies; D007376:Interleukin-2; D017260:Receptor-CD3 Complex, Antigen, T-Cell; D017871:Calcium-Calmodulin-Dependent Protein Kinases