molecular mimicry


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molecular mimicry

Immunology A mechanism that may explain some forms of autoimmune disease, where the immune system attacks self antigens that are structurally similar to nonself antigens
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

molecular mimicry

(mĭm′ĭk-rē)
Antigenic similarity between molecules found on some disease-causing microorganisms and on specific previously healthy body cells or tissues. Molecular mimicry is one explanation for autoimmune diseases. After infection with a microorganism whose surface contains antigens similar to those found in the body, the immune system may respond inappropriately by trying to damage these cells with similar surface antigens in otherwise healthy joints, blood vessels, or other organs.
Medical Dictionary, © 2009 Farlex and Partners
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Reddy, "Relevance of molecular mimicry in the mediation of infectious myocarditis," Journal of Cardiovascular Translational Research, vol.
Roles of Host Immunity in Viral Myocarditis and Dilated Cardiomyopathy
Molecular mimicry and autoimmune liver disease: virtuous intentions, malign consequences.
Cytomegalovirus triggering autoimmune hepatitis: case report and literature review
The objective of this study was to verify the presence of the phenomenon of molecular mimicry between periodontal pathogens with human proteins.
GAKG-RGEKG an Epitope That Provokes Immune Cross-Reactivity between Prevotella sp. and Human Collagen: Evidence of Molecular Mimicry in Chronic Periodontitis
Benvenga, "Injections of Clostridium botulinum neurotoxin A may cause thyroid complications in predisposed persons based on molecular mimicry with thyroid autoantigens," Endocrine, vol.
Immunological Reactivity Using Monoclonal and Polyclonal Antibodies of Autoimmune Thyroid Target Sites with Dietary Proteins
Our results supported the molecular mimicry hypothesis and might conclude that CagA antigen shared similar antigenic epitopes with GPIIb/IIIa instead of GPIb.
Effects of cytotoxin-associated gene A (CagA) positive Helicobacter pylori infection on anti-platelet glycoprotein antibody producing B cells in patients with primary idiopathic thrombocytopenic purpura (ITP)
Considering molecular mimicry of human TIR domains as the mechanism for the immune modulatory effect of bacterial TIR containing domain proteins, TcpF's possible targets in the TLR2 dependent pathway are the TIR domains of TLR2, TLR1, TLR6, and MyD88 as well as MAL [4].
The TIR domain containing locus of Enterococcus faecalis is predominant among urinary tract infection isolates and downregulates host inflammatory response
Studies on the Kilham rat virus (KRV) belonging to the same genus have suggested molecular mimicry [134] and initiation of innate immunity in the pancreatic lymph nodes [135].
Type I diabetes mellitus: genetic factors and presumptive enteroviral etiology or protection
The absolute mechanisms involved in pathogenesis of GBS are still unclear; however, the hypothesis put forward for the immunopathogenesis of GBS is the molecular mimicry between lipopolysaccharides (LPS) and ganglioside-like epitopes in host nerve cells, which leads to cross-reactivity of immune response following infection.
Role of cytokines and toll-like receptors in the immunopathogenesis of guillain-barre syndrome
Molecular mimicry refers to sequence similarities between pathogen derived antigens and human or host native peptides such that a cross-reaction occurs.
The role of intracellular organisms in the pathogenesis of inflammatory arthritis
(1994) Molecular mimicry between GQ1b ganglioside and lipopolysaccharide of Campylobacter jejuni isolated from patients with Fisher's syndrome.
Bio-recognition and functional lipidomics by glycosphingolipid transfer technology
Microbial antigens such as the EBV have been implicated to trigger autoimmune diseases via molecular mimicry. This occurs when the host's immune system recognizes amino acid sequences of microbial antigens and self tissue as the same complex.
Epstein-Barr virus & autoimmune disease: the infection connection
Thus, an immune response against self antigens generated by T-cell activation against bacterial antigens (the molecular mimicry model), may account for the clinical observation (32).
Micronucleus analysis in Behqet's disease with and without HLA-B51/HLA-B51 pozitif ve negatif Behcet hastaliginda mikronukleus analizi

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