Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/120887
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: B cells as effectors and regulators of autoimmunity
Author: Mariño, E.
Grey, S.
Citation: Autoimmunity, 2012; 45(5):377-387
Publisher: Taylor & Francis
Issue Date: 2012
ISSN: 0891-6934
1607-842X
Statement of
Responsibility: 
Eliana Mariño and Shane T. Grey
Abstract: A classic understanding of the interplay between B and T cell components of the immune system that drive autoimmunity, where B cells provide an effector function, is represented by systemic lupus erythematosus (SLE), an autoimmune condition characterised by the production of auto-antibodies. In SLE, CD4+T cells provide cognate help to self-reactive B cells, which in turn produce pathogenic auto-antibodies (1). Thus, B cells act as effectors by producing auto-antibody aided by T cell help such that B and T cell interactions are unidirectional. However, this paradigm of B and T cell interactions is challenged by new clinical data demonstrating that B cell depletion is effective for T cell mediated autoimmune diseases including type I diabetes mellitus (T1D) (2), rheumatoid arthritis (3), and multiple sclerosis (4). These clinical data indicate a model whereby B cells can influence the developing autoimmune T cell response, and therefore act as effectors, in ways that extend beyond the production of autoantibody (5). In this review by largely focusing on type I diabetes we will develop a hypothesis that bi-directional B and T interactions control the course of autoimmunity.
Keywords: B cells; autoimmune; type 1 diabetes; NOD mouse; T cells
Rights: © Informa UK, Ltd.
RMID: 0030126003
DOI: 10.3109/08916934.2012.665527
Appears in Collections:Medicine publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.