Apoptosis and Sjögren syndrome.

摘要: Objective: To examine the role of apoptosis in pathogenesis Sjogren syndrome (SS), a chronic autoimmune disease characterized by infiltration mononuclear cells salivary and lacrimal glands, leading to destruction parenchymal tissue. Methods: A detailed search via MEDLINE (PubMed) Biosis, covering period from January 1994 July 2002, was accomplished, combining key terms SS apoptosis. qualitative review articles undertaken obtained information summarized. Results: Apoptosis acinar ductal epithelial glands has been proposed as possible mechanism responsible for impairment secretory function. Apoptotic cell death may be induced either cytotoxic T through release proteases, such perforin granzyme B, or interaction Fas ligand (FasL/CD95L), expressed lymphocytes, with (Apo-1/CD95) on cells. The increased rate result imbalance between down-regulated apoptosis-inhibitor Bcl-2 up-regulated apoptosis-inducer Bax, autocrine and/or paracrine Fas/FasL interaction. Lymphocytes infiltrating are blocked their ability commit apoptosis, despite expression Fas. these explain resistance resulting prolonged production proinflammatory cytokines autoantibodies, well longer survival that late development lymphoma some patients. Studies SS-like sialoadenitis nonobese diabetic (NOD) mice severe combined immunodeficiency (NOD.scid) suggest primary defect initiation resides undergo mediated This first not-immune-mediated phase target is followed lymphocyte-dependent aggression, which leads extensive tissue damage subsequent loss shown other animal models lines vitro. also play extraglandular manifestations SS, interstitial nephritis peripheral CD4+ lymphocytopenia. Conclusions: suggested literature review. better understanding mechanisms allow discovery new therapeutic strategies. By inhibiting programmed death, glandular function should reduced. Semin Arthritis Rheum 33:49-65.