B cells: new ways to inhibit their function in rheumatoid arthritis.
The apparent efficacy of B-cell depletion in autoimmune diseases has increased interest in targeting B cells. One goal of next generation therapies is to develop treatments that block B-cell activation and preserve resting nonautoimmune cells that maintain B cell memory. To do so, one needs to understand how B cells are activated and what receptors and intracellular signaling pathways regulate this process. This paper will summarize B-cell activation pathways and illustrate how these are being targeted in the development of new treatments for rheumatoid arthritis.
Carter
Robert H
RH
Department of Medicine, University of Alabama at Birmingham, 409 LHRB, 701 19th Street South, Birmingham, AL 35294, USA. rcarter@uab.edu
D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology*; D016175:B-Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology*; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007156:Immunologic Memory; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008213:Lymphocyte Activation / Q000187:drug effects*; D008211:Lymphocyte Cooperation; D008297:Male; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D015398:Signal Transduction / Q000502:physiology
D007166:Immunosuppressive Agents