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https://hdl.handle.net/2440/120887
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Type: | Journal article |
Title: | B cells as effectors and regulators of autoimmunity |
Author: | Mariño, E. Grey, S.T. |
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. |
DOI: | 10.3109/08916934.2012.665527 |
Published version: | http://dx.doi.org/10.3109/08916934.2012.665527 |
Appears in Collections: | Aurora harvest 8 Medicine publications |
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