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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1996 Apr 16;93(8):3357–3361. doi: 10.1073/pnas.93.8.3357

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

H Molina 1, V M Holers 1, B Li 1, Y Fung 1, S Mariathasan 1, J Goellner 1, J Strauss-Schoenberger 1, R W Karr 1, D D Chaplin 1
PMCID: PMC39612  PMID: 8622941

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.

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Selected References

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