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Re: “Collagen-Induced Arthritis in TNF Receptor-1-Deficient Mice: TNF Receptor-2 Can Modulate Arthritis in the Absence of TNF Receptor 1”

Clinical Immunology Vol. 99, No. 3, June, pp. 305–307, 2001 doi:10.1006/clim.2001.5030, available online at http://www.idealibrary.com on EDITORIAL Re: “Collagen-Induced Arthritis in TNF Receptor-1-Deficient Mice: TNF Receptor-2 Can Modulate Arthritis in the Absence of TNF Receptor 1” John D. Mountz Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama, 701 South 19th Street, LHRB 473, Birmingham, Alabama 35294 The relative contributions of TNFR1 and TNFR2 signaling in TNF-induced proinflammatory response leading to arthritis as well as an anti-inflammatory or proapoptotic death have been difficult to establish. In T cells, signaling through both TNFR1 and TNFR2 can activate caspase 8, leading to a proapoptotic signal as well as to activation of NF- B, which leads to a proinflammatory, antiapoptotic signal. Signaling through TNFR1 couples to the apoptosis pathway through the adapter molecules TNF receptor-associated death domain (TRADD) and Fas-associated death domain (FADD) to dock with caspase 8 (1–3) (Fig. 1). Similarly, signaling through TNFR2 signals through TRAF2, which leads to recruitment of RIP3 (4). The death domain of RIP3 binds to FADD, which activates caspase 8, leading to apoptosis signaling (5). TNFR1 apoptosis signaling occurs in many cell types, whereas TNFR2 apoptosis signaling is more restricted to http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Immunology Elsevier
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