RGD Reference Report - Increased activation of the alternative complement pathway in sickle cell disease. - Rat Genome Database

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Increased activation of the alternative complement pathway in sickle cell disease.

Authors: Chudwin, DS  Korenblit, AD  Kingzette, M  Artrip, S  Rao, S 
Citation: Chudwin DS, etal., Clin Immunol Immunopathol. 1985 Oct;37(1):93-7.
RGD ID: 11040777
Pubmed: PMID:3896597   (View Abstract at PubMed)

Complement proteins play an important role in host defenses against Streptococcus pneumoniae, a major cause of serious infections in sickle cell (SS) disease. Previous studies have suggested abnormalities of the alternative complement pathway in SS disease. We measured activation of the alternative pathway in sera from patients with SS disease utilizing an enzyme immunoassay which detects C3b,P complexes, derivative of the C3b,Bb,P alternative pathway convertase. In all, 89% of SS sera had elevated concentrations of C3b,P complexes, indicative of increased alternative pathway activation. Chronic activation of the alternative pathway may contribute to impaired host defense in SS patients.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
C3Ratsickle cell anemia severityISOC3 (Homo sapiens) RGD 
C3Mousesickle cell anemia severityISOC3 (Homo sapiens) RGD 
C3Humansickle cell anemia severityIEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
C3  (complement C3)

Genes (Mus musculus)
C3  (complement component 3)

Genes (Homo sapiens)
C3  (complement C3)

Objects referenced in this article
Gene C5 complement C5 Homo sapiens
Gene Hc hemolytic complement Mus musculus
Gene C5 complement C5 Rattus norvegicus

Additional Information