dgn-np:NP791085.RAgltq5YWfFdSTVvYVFUXsIO-3Z_GrDx_zBjjZgPO_tvQ130_provenance {
  dgn-np:NP791085.RAgltq5YWfFdSTVvYVFUXsIO-3Z_GrDx_zBjjZgPO_tvQ130_assertion dcterms:description "[Although many of these recently described models of intestinal inflammation have not been thoroughly investigated, several consistent features are present which provide important insights into the role of cytokines in the pathogenesis of intestinal inflammation: (i) entirely distinct genetic alterations of cytokine expression and T-lymphocyte activity can lead to phenotypically similar intestinal inflammation, suggesting that human inflammatory bowel disease could have marked genetic heterogeneity; (ii) dysregulation of any of a number to immunoregulatory molecules can result in intestinal inflammation, illustrating the complexity of the mucosal immune response; (iii) active immunosuppression is critical to maintaining mucosal homeostasis; (iv) interferon-gamma and CD4+ lymphocytes, probably of the TH1 phenotype, are required for progression of chronic intestinal inflammation; (v) monokines are consistently upregulated, but tumour necrosis factor blockade is only partially protective.]. 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:8899099 ;
    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 .
}