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

Academic Article

Abstract

  • 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.
  • Digital Object Identifier (doi)

    Author List

  • Molina H; Holers VM; Li B; Fang YF; Mariathasan S; Goellner J; Strauss-Schoenberger J; Karr RW; Chaplin DD
  • Start Page

  • 3357
  • End Page

  • 3361
  • Volume

  • 93
  • Issue

  • 8