RGD Reference Report - Cutting edge: myeloid complement C3 enhances the humoral response to peripheral viral infection. - Rat Genome Database

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Cutting edge: myeloid complement C3 enhances the humoral response to peripheral viral infection.

Authors: Verschoor, A  Brockman, MA  Knipe, DM  Carroll, MC 
Citation: Verschoor A, etal., J Immunol. 2001 Sep 1;167(5):2446-51.
RGD ID: 7401276
Pubmed: PMID:11509581   (View Abstract at PubMed)

HSV-1 is the causative agent of cutaneous lesions, commonly referred to as cold sores. Primary exposure to the virus ordinarily occurs through the periphery, in particular through abraded skin or mucosal membranes. Under certain circumstances (e.g., in neonatals or AIDS patients), the infection becomes disseminated, often with severe consequences. Spread of HSV-1 is limited by virus-specific Ab. The development of an efficient humoral response to the virus is dependent on innate immunity component complement C3. The liver is the major source of C3, but there are also extrahepatic origins of C3 such as lymphoid macrophages. In the present study, the significance of C3 synthesis by bone marrow-derived cells was assessed by the transfer of wild-type bone marrow into irradiated C3-deficient mice. Using these chimeric mice, extrahepatic C3 was determined sufficient to initiate specific Ab and memory responses to a peripheral HSV-1 infection.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
C3Ratherpes simplex  ISOC3 (Mus musculus) RGD 
C3Mouseherpes simplex  IMP  RGD 
C3Humanherpes simplex  ISOC3 (Mus musculus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
C3  (complement C3)

Genes (Mus musculus)
C3  (complement component 3)

Genes (Homo sapiens)
C3  (complement C3)


Additional Information