dgn-np:NP500742.RA59j-6vx1hXDj2PGFrW9U_fJApDspxvm37tz0aEPDdRg130_provenance {
  dgn-np:NP500742.RA59j-6vx1hXDj2PGFrW9U_fJApDspxvm37tz0aEPDdRg130_assertion dcterms:description "[Evidence for the following conclusion about this model, and by implication about human ANCA disease, will be summarized as follows: (1) anti-MPO IgG is sufficient even in the absence of functional T cells to cause disease and anti-MPO T lymphocytes are not sufficient to cause acute injury; (2) neutrophils are required; (3) ANCA antigens in bone marrow-derived cells are sufficient targets; (4) increased circulating pro-inflammatory cytokines and microbial products exacerbate disease, and concurrent viral infection exacerbates and modulates the phenotype of disease; (5) Fcγ receptor engagement is required for disease induction, and Fcγ receptor repertoire modulates the phenotype of disease, especially pulmonary disease; (6) activation of the alternative pathway of complement is required, complement is activated by factors released by neutrophils stimulated by ANCA IgG and engagement of C5a receptors is a primary event in complement-mediated amplification; and (7) genetic background has a marked influence on the severity and outcome of disease, and modified gene expression in bone marrow-derived cells is the primary basis for genetically determined differences in disease susceptibility.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ;
    wi:evidence dgn-void:source_evidence_literature ;
    sio:SIO_000772 miriam-pubmed:21252521 ;
    prov:wasDerivedFrom dgn-void:befree-20140225 ;
    prov:wasGeneratedBy eco:ECO_0000203 .
  dgn-void:befree-20140225 pav:importedOn "2014-02-25"^^xsd:date .
  dgn-void:source_evidence_literature a eco:ECO_0000212 ;
    rdfs:comment "Gene-disease associations inferred from text-mining the literature."@en ;
    rdfs:label "DisGeNET evidence - LITERATURE"@en .
}