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.
Skip Nav Destination
Article navigation
January 2018
-
Cover Image
Cover Image
Oleic-acid-treated HepG2 cells immunostained for PGC-1α (PPARγ co-activator-1 α). In Clinical Science volume 132, issue 1, the results of work by Bernardi et al. include reporting that the protein TRAIL (TNF-related apoptosis inducing ligand) increases the expression of PGC-1α in HepG2 cells cultured with oleic acid. Overall, the article points to a potential therapeutic role for TRAIL against impaired glucose tolerance and non-alcoholic fatty liver disease; for details see pages 69–83.
Review Article|
January 05 2018
The molecular basis of immune regulation in autoimmunity
Shu-Han Yang;
Shu-Han Yang
1Chronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou 510006, China
2Liver Immunology Laboratory, Institute of Immunology and School of Life Sciences, University of Science and Technology of China, Hefei 230027, China
Search for other works by this author on:
Cai-yue Gao;
Cai-yue Gao
1Chronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou 510006, China
2Liver Immunology Laboratory, Institute of Immunology and School of Life Sciences, University of Science and Technology of China, Hefei 230027, China
Search for other works by this author on:
Liang Li;
Liang Li
1Chronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou 510006, China
2Liver Immunology Laboratory, Institute of Immunology and School of Life Sciences, University of Science and Technology of China, Hefei 230027, China
Search for other works by this author on:
Christopher Chang;
Christopher Chang
3Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA, U.S.A.
Search for other works by this author on:
Patrick S.C. Leung;
3Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA, U.S.A.
Correspondence: Zhe-Xiong Lian ([email protected]) or Patrick S.C. Leung ([email protected]) or M. Eric Gershwin ([email protected])
Search for other works by this author on:
M. Eric Gershwin;
3Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA, U.S.A.
Correspondence: Zhe-Xiong Lian ([email protected]) or Patrick S.C. Leung ([email protected]) or M. Eric Gershwin ([email protected])
Search for other works by this author on:
Zhe-Xiong Lian
1Chronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou 510006, China
2Liver Immunology Laboratory, Institute of Immunology and School of Life Sciences, University of Science and Technology of China, Hefei 230027, China
Correspondence: Zhe-Xiong Lian ([email protected]) or Patrick S.C. Leung ([email protected]) or M. Eric Gershwin ([email protected])
Search for other works by this author on:
Publisher: Portland Press Ltd
Received:
October 14 2017
Revision Received:
November 21 2017
Accepted:
November 27 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2018 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2018
Clin Sci (Lond) (2018) 132 (1): 43–67.
Article history
Received:
October 14 2017
Revision Received:
November 21 2017
Accepted:
November 27 2017
Citation
Shu-Han Yang, Cai-yue Gao, Liang Li, Christopher Chang, Patrick S.C. Leung, M. Eric Gershwin, Zhe-Xiong Lian; The molecular basis of immune regulation in autoimmunity. Clin Sci (Lond) 16 January 2018; 132 (1): 43–67. doi: https://doi.org/10.1042/CS20171154
Download citation file:
Sign in
Don't already have an account? Register
Sign in to your personal account
You could not be signed in. Please check your email address / username and password and try again.
Could not validate captcha. Please try again.
Biochemical Society Member Sign in
Sign InSign in via your Institution
Sign in via your InstitutionGet Access To This Article
Open Access for all
We offer compliant routes for all authors from 2025. With library support, there will be no author nor reader charges in 5 journals. Check here |
![]() |