B cell contribution of the CD4+ T cell inflammatory phenotypes in systemic lupus erythematosus. (2nd January 2017)

• Record Type: Journal Article
• Authors: Choi, Seung-Chul; Morel, Laurence
• Is Part Of: Autoimmunity. Volume 50:Number 1(2017)
• Page Start: 37
• Page End: 41
• Publication Date: 2017-01-02
• Subjects: Follicular helper T cells -- Th17 -- Treg -- B1-a cells -- marginal zone B cells; Autoimmunity -- Periodicals; Autoimmune diseases -- Periodicals; 571.973
• DOI: 10.1080/08916934.2017.1280028
• Languages: English
• ISSNs: 0891-6934

Abstract

Abstract: Systemic lupus erythematosus is an autoimmune disease in which the effector molecules responsible for tissue damage are antibodies directed against a large number of self-antigens, among which nucleic acids complexed with proteins play a prominent role. These pathogenic autoantibodies are produced by plasma cells differentiated from activated autoreactive B cells, a process that requires complex interactions between multiple components of the immune systems. A key step in the activation of autoreactive B cells is provided by CD4 + T cells through cytokines and cell-to-cell contact. Lupus CD4 + T cells are autoreactive and they present an activated inflammatory phenotype that has been shown to contribute to disease. In addition to their role in antibody production, B cells have other effector functions, the most important ones being antigen presentation to and co-stimulation of CD4 + T cells, as well as the secretion of cytokines. Here, we review what is known, largely based on mouse models, how these B cell effector functions contribute to the CD4 + T cell inflammatory phenotypes in lupus. When possible, we compare CD4 + T cell activation by B cells and by dendritic cells, and speculate how these interactions may contribute to the disease process.