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NF-kB, nuclear facotr k|3; ALPS, autoimmune lymphoproliferative syndrome.

NF-kB, nuclear facotr k|3; ALPS, autoimmune lymphoproliferative syndrome.

molecular mimicry (i.e., presentation and recognition of cryptic epitopes of self-antigens). Further downstream, execution of immune responses depends on cooperation of many cell types, cytokines, and intracellular signaling networks. Therefore, autoimmunity represents the end result of the breakdown of one or more of the basic mechanisms of immune tolerance (Table 1).

Autoimmunity may occur in normal individuals, with a higher frequency in older people. Infectious diseases often elicit autoreactivities based on similarity between exogenous and self-antigens. Infection-induced autoimmunity usually is self-limited by elimination of the antigen-producing cell or organism. However, self-reactivity may be sustained through molecular mimicry (1) (i.e., homology between exogenous and endogenous epitopes) and the inability of the immune system to destroy self-reactive B or T cells via apoptosis, anergy, or other regulatory mechanisms. Nevertheless, autoimmunity does not necessarily lead to tissue injury. Autoantibodies, such as rheumatoid factor or antinuclear antibodies occur in more than 5% of normal subjects without ever resulting in rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE), which are characterized by the very presence of such antibody reactivities.

Table 2

Systemic Autoimmune Diseases

Table 2

Systemic Autoimmune Diseases

Disease

Organ system involvement and immunopathology

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