title: Altered B-cell signaling in lupus.
abstract: Systemic lupus erythematosus (SLE) is an autoimmune disease of complex etiology primarily characterized by the presence of high titers of autoantibodies targeting many nuclear as well as cytoplasmic antigens, with resultant end-organ damage. Aberrant signaling events have been documented in various lymphocyte populations, and they have constituted attractive targets for therapeutic intervention. Murine models of lupus (conventional or engineered) have yielded interesting snapshots of the signaling status of lupus lymphocytes, and many of these alterations in cell signaling observed in murine models of lupus have also been documented in patient samples. Analyses of B-cell signaling in various murine lupus models have not only provided an in-depth perspective of the signaling status and possibly the underlying mechanisms leading to enhanced survival of autoimmune B cells, but have also presented us with potential strategies for treating lupus.
authors: Division of Rheumatology, and Center for Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-8884, USA. Kui.Liu@utsouthwestern.edu
authors: Kui
authors: K
authors: Liu
authors: Chandra
authors: C
authors: Mohan
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified / Q000235:genetics / Q000276:immunology*; D015551:Autoimmunity / Q000235:genetics / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D002470:Cell Survival / Q000235:genetics / Q000276:immunology; D004195:Disease Models, Animal; D018390:Gene Targeting / Q000379:methods / Q000639:trends; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000235:genetics / Q000378:metabolism* / Q000628:therapy; D051379:Mice; D012107:Research Design; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology