Immune cell signaling in lupus

Citation
Gc. Tsokos et al., Immune cell signaling in lupus, CURR OP RH, 12(5), 2000, pp. 355-363
Citations number
60
Categorie Soggetti
Rheumatology
Journal title
CURRENT OPINION IN RHEUMATOLOGY
ISSN journal
10408711 → ACNP
Volume
12
Issue
5
Year of publication
2000
Pages
355 - 363
Database
ISI
SICI code
1040-8711(200009)12:5<355:ICSIL>2.0.ZU;2-C
Abstract
The fate of the lymphocyte is determined by integration of signals delivere d after the binding of antigen to the surface antigen receptor, signals del ivered by cytokines that bind to their surface receptors, and signals initi ated after the engagement of other surface receptors, known as costimulator y molecules. The summation of this input determines whether the immune cell will become stimulated, ignore the signal (anergy), or die (apoptosis). An tigen-receptor signaling events are abnormal in lupus lymphocytes, manifest ed by increased calcium responses and hyperphosphorylation of several cytos olic protein substrates. Further down, at the gene transcription level, the activity of the nuclear factor kappa B is decreased. These events are unde rwritten by defective T cell receptor zeta chain expression, overexpression of the gamma chain of the Fc epsilon RI that functions as an alternate of zeta chain, and decreased p65 -Rel A protein that is responsible for the in ducible NF kappa B activity, Accumulated research data have enabled us to b egin deciphering the molecular basis of the abnormal lupus lymphocyte and m ay lead to the development of new medicinal treatments for lupus. (C) 2000 Lippincoit Williams & Wilkins, Inc.