Int. J. Environ. Res. Public Health 2004, 1(1), 39-73; doi:10.3390/ijerph2004010039
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Molecular and Cellular Mechanisms Associated with Autoimmune Diseases

Received: 30 October 2003; Accepted: 15 January 2004 / Published: 29 February 2004
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: 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
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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.

AMA Style

Ayensu WK, Tchounwou PB, McMurray RW. Molecular and Cellular Mechanisms Associated with Autoimmune Diseases. International Journal of Environmental Research and Public Health. 2004; 1(1):39-73.

Chicago/Turabian Style

Ayensu, Wellington K.; Tchounwou, Paul B.; McMurray, Robert W. 2004. "Molecular and Cellular Mechanisms Associated with Autoimmune Diseases." Int. J. Environ. Res. Public Health 1, no. 1: 39-73.

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