Immune cell signaling defects in lupus: activation, anergy and death.
Recent studies have identified novel aberrations in antigen receptor-mediated signaling events in lymphocytes from patients with systemic lupus erythematosus. Here, we propose that in lupus lymphocytes, the receptor-mediated increase in protein tyrosine phosphorylation and cytoplasmic free Ca2+ responses, along with T-cell receptor zeta chain deficiency, might explain the previously described diverse and conflicting immunoregulatory defects in human lupus.
Tsokos
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GC
Uniformed Services University of the Health Sciences, Dept of Medicine, Bethesda, MD 20814, USA. gtsokos@usa.net
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D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D017635:Clonal Anergy / Q000276:immunology*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology*; D008214:Lymphocytes / Q000276:immunology*; D011947:Receptors, Antigen, B-Cell / Q000172:deficiency / Q000276:immunology*; D011948:Receptors, Antigen, T-Cell / Q000172:deficiency / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology*
D011947:Receptors, Antigen, B-Cell; D011948:Receptors, Antigen, T-Cell