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

J Immunol. 2001 Sep 1;167(5):2446-51. doi: 10.4049/jimmunol.167.5.2446.


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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies, Viral / biosynthesis*
  • Bone Marrow Cells / immunology*
  • Bone Marrow Transplantation / immunology
  • Bone Marrow Transplantation / pathology
  • Chimera / immunology
  • Complement C3 / deficiency
  • Complement C3 / genetics
  • Complement C3 / metabolism*
  • Herpes Simplex / immunology*
  • Herpes Simplex / pathology
  • Herpesvirus 1, Human / immunology
  • Humans
  • Infant, Newborn
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout


  • Antibodies, Viral
  • Complement C3