Next Article in Journal
Association of Clinical Complications with Nutritional Status and the Prevalence of Leukopenia among Arsenic Patients in Bangladesh
Previous Article in Journal
Toxicity of a Mixture of 2,4-Dichlorophenoxyacetic Acid and Mono-soduim Methanearsonate to the Red Swamp Crawfish, Procambarus clarkii
Article Menu

Article Versions

Export Article

Open AccessReview
Int. J. Environ. Res. Public Health 2004, 1(1), 39-73;

Molecular and Cellular Mechanisms Associated with Autoimmune Diseases

Cellomics and Toxicogenomics Research Laboratory, NIH-Center for Environmental Health, College of Science, Engineering, and Technology, Jackson State University, 1400 Lynch Street, Box 18540, Jackson, Mississippi 39217, USA
Rheumatology Section, G.V. (Sonny) Montgomery V.A. Hospital, and Division of Rheumatology and Molecular Immunology, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA
Author to whom correspondence should be addressed.
Received: 30 October 2003 / Accepted: 15 January 2004 / Published: 29 February 2004
PDF [700 KB, uploaded 19 June 2014]


Evidence points to increases in the incidence and prevalence of several autoimmune diseases in the United States. As a result, the cost to public health from clinical management of autoimmune conditions is on the rise. The initiation and progression of autoimmune disturbances involves both genetic and environmental factors. Deficiencies in important proteins that normally participate in maintaining checks and balances within the internal milieu may render an individual prone to developing autoantibodies. Structural abnormalities or decline in normal levels of the pentraxins (serum amylase-P protein, the acute phase proteins, complement, and C-reactive proteins) have been shown to induce autoimmunity. Irregular transmission of information arising from multiple signal transduction pathways typically associated with the serine/threonine cascade routes of mitogen activating phosphorylation kinases, has also been found to induce autoimmunity. The kind of ligand/receptor interactions drives physical recruitment of different signals within the lymphocyte; these links define the quality and quantity of subsequent immune responses. CD95 or the Fas/Apo-1 and its ligand CD95L participate in regulating lymphocyte populations and therefore influence various aspects of immune responses. Mutational abnormalities resulting from synthesis of proteins by the CD95 and/or its ligand CD95L may result in alterations in the apoptotic pathways. Apoptosis may be completely inhibited, activated or partially stimulated. Modulation of apoptosis may lead to accumulation of self-antigens. Subsequently the immune system may be stimulated to react against self-molecules through lymphatic hyperplasia. This process may end up in proliferative disorders and enhanced susceptibility to autoimmune syndromes. This paper deals with mechanisms of autoimmunopathogenesis at the cellular and molecular levels. Emphasis is laid on the role of T and B cell receptor/ligand interactions, functions and malfunctions due to structural and quantitative alterations in T- B- cell cluster of antigen determinants. Genetically susceptible patients who develop spontaneous autoimmune diseases are examined and the etiological factors implicated in the initiation and subsequent dissemination of autoimmune diseases is discussed.
Keywords: self-tolerance; T cell receptor; B cell receptor; autoimmunopathogenesis; apoptosis self-tolerance; T cell receptor; B cell receptor; autoimmunopathogenesis; apoptosis
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Share & Cite This Article

MDPI and ACS Style

Ayensu, W.K.; Tchounwou, P.B.; McMurray, R.W. Molecular and Cellular Mechanisms Associated with Autoimmune Diseases. Int. J. Environ. Res. Public Health 2004, 1, 39-73.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Environ. Res. Public Health EISSN 1660-4601 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top