Fas (CD95)-related apoptosis and rheumatoid arthritis.
Abnormal proliferation and/or persistence of synoviocytes and inflammatory cells has long been described in inflammatory arthritis conditions, but only relatively recently has substantial attention been drawn to the relevance of abnormal apoptotic processes in disease pathogenesis and treatment. This review summarizes a current understanding of the Fas (CD95)-Fas ligand (CD178) apoptotic system, which has most predominantly been examined in rheumatoid arthritis. There, synovial inflammation is often characterized by a unique resistance to Fas-related apoptosis, and agonistic therapeutic interventions upon Fas have consistently been found beneficial in both animal and human disease models. Therefore, modulation of the Fas pathway will hopefully be of both pathogenic and therapeutic interest in the study of inflammatory arthritis conditions in general.
Peng
S L
SL
Inflammation, Autoimmunity and Transplantation Research, Roche Palo Alto, CA 94025, USA. stanford.peng@roche.com
D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000628:therapy; D016207:Cytokines / Q000276:immunology; D053222:Fas Ligand Protein; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology*; D023421:Models, Animal; D013583:Synovial Membrane / Q000276:immunology; D048069:Tumor Necrosis Factors / Q000502:physiology*; D019014:fas Receptor / Q000502:physiology*
D016207:Cytokines; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D048069:Tumor Necrosis Factors; D019014:fas Receptor