| Literature DB >> 29305419 |
Shu-Han Yang1,2, Cai-Yue Gao1,2, Liang Li1,2, Christopher Chang3, Patrick S C Leung4, M Eric Gershwin4, Zhe-Xiong Lian5,2.
Abstract
Autoimmune diseases can be triggered and modulated by various molecular and cellular characteristics. The mechanisms of autoimmunity and the pathogenesis of autoimmune diseases have been investigated for several decades. It is well accepted that autoimmunity is caused by dysregulated/dysfunctional immune susceptible genes and environmental factors. There are multiple physiological mechanisms that regulate and control self-reactivity, but which can also lead to tolerance breakdown when in defect. The majority of autoreactive T or B cells are eliminated during the development of central tolerance by negative selection. Regulatory cells such as Tregs (regulatory T) and MSCs (mesenchymal stem cells), and molecules such as CTLA-4 (cytotoxic T-lymphocyte associated antigen 4) and IL (interleukin) 10 (IL-10), help to eliminate autoreactive cells that escaped to the periphery in order to prevent development of autoimmunity. Knowledge of the molecular basis of immune regulation is needed to further our understanding of the underlying mechanisms of loss of tolerance in autoimmune diseases and pave the way for the development of more effective, specific, and safer therapeutic interventions.Entities:
Keywords: Autoreactive lymphocytes; Immune tolerance; T regulatory cells; autoimmunity; immunomodulation; molecular basis of health and disease
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Year: 2018 PMID: 29305419 DOI: 10.1042/CS20171154
Source DB: PubMed Journal: Clin Sci (Lond) ISSN: 0143-5221 Impact factor: 6.124