Antibody Cross-Reactivity in Auto-Immune Diseases

被引:17
作者
Trier, Nicole Hartwig [1 ]
Houen, Gunnar [1 ,2 ]
Murdaca, Giuseppe
机构
[1] Rigshosp Glostrup, Dept Neurol, Valdemar Hansens Vej 1-23, DK-2600 Glostrup, Denmark
[2] Univ Southern Denmark, Dept Biochem & Mol Biol, Campusvej 55, DK-5230 Odense, Denmark
关键词
autoantibody; autoimmunity; cross-reactivity; epitopes; infections; molecular mimicry; virus; EPSTEIN-BARR-VIRUS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RHEUMATOID-ARTHRITIS PATIENTS; DIABETES-ASSOCIATED AUTOANTIBODIES; CITRULLINATED PROTEIN ANTIBODIES; MYELIN BASIC-PROTEIN; T-CELL-CLONES; MOLECULAR MIMICRY; MULTIPLE-SCLEROSIS; MONOCLONAL-ANTIBODY;
D O I
10.3390/ijms241713609
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autoimmunity is defined by the presence of antibodies and/or T cells directed against self-components. Although of unknown etiology, autoimmunity commonly is associated with environmental factors such as infections, which have been reported to increase the risk of developing autoimmune diseases. Occasionally, similarities between infectious non-self and self-tissue antigens may contribute to immunological cross-reactivity in autoimmune diseases. These reactions may be interpreted as molecular mimicry, which describes cross-reactivity between foreign pathogens and self-antigens that have been reported to cause tissue damage and to contribute to the development of autoimmunity. By focusing on the nature of antibodies, cross-reactivity in general, and antibody-antigen interactions, this review aims to characterize the nature of potential cross-reactive immune reactions between infectious non-self and self-tissue antigens which may be associated with autoimmunity but may not actually be the cause of disease onset.
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页数:23
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