This is a mechanism module, not a specific disease. Disorder entries reference individual nodes via conforms_to (e.g., "molecular_mimicry_autoimmunity#Cross-Reactive Autoreactive Lymphocyte Activation"). The module defines the expected pathophysiology structure; conforming nodes in disorder files should include the corresponding cell types, biological processes, and causal edges, specialized to their disease context. Key disorder-specific substitutions of the mimic pair: Guillain-Barre syndrome uses Campylobacter jejuni sialylated lipo-oligosaccharide mimicking peripheral-nerve gangliosides (anti-GM1/GD1a/GQ1b); MIS-C uses a SARS-CoV-2 nucleocapsid epitope mimicking the host antiviral-signalling protein SNX8; acute rheumatic fever (not yet a worked conformer) uses streptococcal M protein mimicking cardiac myosin. Susceptibility is frequently gated by HLA alleles that provide the restricting element for presentation of the cross-reactive epitope. Mimic chemistry and specific autoantigens are described in prose only; modules bind GO and CL terms only and do not use gene (HGNC) or chemical (CHEBI) term bindings.
Infection-Associated Cross-Reactive Antigen Exposure
trigger
An infectious agent (or, less commonly, a chemical/environmental antigen) presents an epitope that shares sequence or structural similarity with a host self-antigen. Antigen processing and presentation of this foreign epitope in a susceptible host is the initiating event: because the foreign and self peptides are similar, the immune response mounted against the pathogen is positioned to cross-react with self. The specific mimic pair is disorder-specific (e.g., Campylobacter lipo-oligosaccharide vs nerve gangliosides; SARS-CoV-2 nucleocapsid vs SNX8).
Downstream
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Cross-Reactive Autoreactive Lymphocyte Activation
Cross-Reactive Autoreactive Lymphocyte Activation
central effector
The anti-pathogen response activates autoreactive T and/or B lymphocytes whose receptors recognize both the foreign epitope and the mimicked self-antigen. These cross-reactive clones escaped central tolerance and are expanded by the foreign-derived antigen; cross-reactive B cells secrete autoantibodies and cross-reactive T cells acquire effector function. This is the pivotal, conserved step that converts a normal antimicrobial response into autoreactivity, and is the canonical conformance target for disorders driven by molecular mimicry.
Downstream
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Autoreactive Effector-Mediated Tissue Injury
Epitope Spreading and Autoimmune Amplification
amplifier
Effector-mediated tissue damage releases previously sequestered self-antigens that are taken up and presented, priming additional self-reactive T and B clones directed at epitopes distinct from the original mimic (epitope spreading). Together with breach of central tolerance, bystander activation, and persistent antigenic stimulation, this broadens and perpetuates the autoimmune response independent of ongoing infection, converting an initially antigen-restricted reaction into a self-sustaining one.
Downstream
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Tissue-Specific Autoimmune Disease
Tissue-Specific Autoimmune Disease
consequence
The cumulative cross-reactive and spread autoimmune attack produces clinical disease localized to the tissue expressing the mimicked self-antigen, with the syndrome defined by which tissue is targeted (e.g., acute polyradiculoneuropathy in Guillain-Barre syndrome, multisystem hyperinflammation in MIS-C, carditis in rheumatic fever). This is the clinical consequence of the conserved molecular-mimicry chain and the level at which conforming disorder entries are defined.