SLE - Rituximab in lupus 英文参考文献.docVIP

Available online /content/5/4/157 Commentary SLE Rituximab in lupus Robert Eisenberg Division of Rheumatology, University of Pennsylvania, Philadelphia, Pennsylvania, USA Corresponding author: Robert Eisenberg (e-mail: raemd@) Received: 5 Mar 2003 Accepted: 17 Mar 2003 Published: 15 Apr 2003 Arthritis Res Ther 2003, 5:157-159 (DOI 10.1186/ar759) ? 2003 BioMed Central Ltd (Print ISSN 1478-6354; Online ISSN 1478-6362) Abstract B cells are essential to the development of systemic lupus erythematosus (SLE). The chimeric monoclonal antibody rituximab depletes B cells by targeting the pan-B-cell surface marker CD20. Preliminary experience with this agent in SLE and other autoimmune diseases has been encouraging. Controlled trials in SLE will be necessary to determine whether rituximab is useful therapy in this disease, and will teach us more about the roles of B cells in its pathogenesis. Keywords: B cells, CD20, rituximab, systemic lupus erythematosus Introduction: B cells in systemic lupus Other studies in mice genetically without B cells also implicate B cells in a number of immunoregulatory interac- tions that go beyond their clear role as the precursor of antibody forming cells [6]. B cells can regulate T cells, dendritic cells and other B cells. They can produce a variety of cytokines, including IL-4 and IL-10, and even can differentiate into subtypes that secrete certain sets of cytokines, analogous to T helper type 1 and T helper type 2 cells [7]. B cells are superb antigen presenting cells, since they can express MHC class II as well as co- stimulatory molecules such as CD80 and CD86, and their cell surface immunuoglobulin antigen receptor is ideal for focusing and concentrating specific protein molecules [8]. erythematosus A central feature of systemic lupus erythematosus (SLE) is the loss of B-cell tolerance. At least some autoant