The basis of autoimmunity: Part I mechanisms of aberrant self-recognition

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Abstract

In this two-part series, Argyrios N. Theofilopoulos summarizes the current state of affairs in the field of autoimmunity. Part I integrates the collective mechanistic theories of autoimmune diseases. The most straightforward explanation to emerge with regard to organ-specific diseases is the concept that these are caused by inappropriate, yet conventional, immunological responses against self-antigens for which tolerance has never been established. A similar mechanism may be operative in systematic autoimmunity, but other abnormalities such as defects in the apoptosis machinery may also be invoked. Part II will address the genetic contributions predisposing to autoimmune syndromes.

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      Citation Excerpt :

      Among other immune challenges the number of studies are small and the results ambiguous (Table 5), although it can be noted that both studies measuring the bacteria-killing activity in the blood reported enhanced innate responses in the carotenoid-supplemented group. One drawback of the vertebrate immune system is the risk of autoimmune reactions, that is when the organism's own immune system mistakenly identifies self-antigens as foreign and elicits responses against the organism's own cells (Theofilopoulos 1995). The severe consequences of autoimmune reactions and diseases are well known in humans, mice, Mus musculus, and chickens, Gallus gallus domesticus (Goldsby et al. 2003; Erf 2008).

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    The author thanks M. Duchosal, S.R. Duncan, D.H. Kono, D. Lo, P. Peterson, R. Rubin, J. Sprent and W. Weigle for critically reviewing the manuscript. The work of the author is supported by US National Institutes of Health grants AR31203 and AR39555.

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    Argyrios N. Theofilopoulos is at the Dept of Immunology. The Scripps Research Institute, 10666 North Torrey Pines Road/IMM3, La Jolla, CA 92037, USA.

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