The role of apoptosis in Sjögren's syndrome.
It has been suggested that defects in the modulation of programmed cell death/apoptosis might lead to autoimmune disease, such as Sjögren's syndrome (SS) and systemic lupus erythematosus. In this review some basic information on apoptosis is introduced together with three aspects on apoptosis in relation to SS: i) defective apoptosis could lead to lymphoid cell accumulation and chronic inflammation in exocrine glands; ii) increased apoptosis of epithelial cells might explain the loss of secreting epithelium; and iii) orderly destruction of cellular components might induce autoantibody production. Altogether, the idea that defects in the apoptotic process could be of importance for explaining autoimmune diseases, makes research on the different factors in this pathway valuable for achieving a better understanding of the etiopathogenesis of SS.
Bolstad
A I
AI
Broegelmann Research Laboratory, Armauer Hansen Bldg, University of Bergen and Haukeland University Hospital, N-5021 Bergen, Norway.
Jonsson
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R
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001323:Autoantibodies / Q000276:immunology; D004847:Epithelial Cells / Q000276:immunology / Q000473:pathology; D005088:Exocrine Glands / Q000276:immunology / Q000473:pathology; D053222:Fas Ligand Protein; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D008562:Membrane Glycoproteins / Q000502:physiology; D051379:Mice; D012859:Sjogren's Syndrome / Q000276:immunology / Q000473:pathology*; D019014:fas Receptor / Q000502:physiology
D001323:Autoantibodies; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D019014:fas Receptor