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Markedly impaired humoral immune response in mice deficient in complement receptors 1 and 2.

Complement receptor 1 (CR1, CD35) and complement receptor 2 (CR2, CD21) have been implicated as regulators of B-cell activation. We explored the role of these receptors in the development of humoral immunity by generating CR1- and CR2-deficient mice using gene-targeting techniques. These mice have normal basal levels of IgM and of IgG isotypes. B- and T-cell development are overtly normal. Nevertheless, B-cell responses to low and high doses of a T-cell-dependent antigen are impaired with decreased titers of antigen-specific IgM and IgG isotypes. This defect is not complete because there is still partial activation of B lymphocytes during the primary immune response, with generation of splenic germinal centers and a detectable, although reduced, secondary antibody response. These data suggest that certain T-dependent antigens manifest an absolute dependence on complement receptors for the initiation of a normally robust immune response.

Pubmed ID: 8622941


  • Molina H
  • Holers VM
  • Li B
  • Fung Y
  • Mariathasan S
  • Goellner J
  • Strauss-Schoenberger J
  • Karr RW
  • Chaplin DD


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

April 16, 1996

Associated Grants

  • Agency: NIAID NIH HHS, Id: AI31105
  • Agency: NIAMS NIH HHS, Id: ARO1910-01

Mesh Terms

  • Animals
  • Antibody Formation
  • B-Lymphocytes
  • Erythrocytes
  • Gene Targeting
  • Immunization
  • Immunoglobulin G
  • Immunoglobulin M
  • Lymphocyte Activation
  • Mice
  • Mice, Knockout
  • Receptors, Complement 3b
  • Receptors, Complement 3d
  • Sheep
  • T-Lymphocytes