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Markedly Impaired Humoral Immune Response in Mice Deficient in Complement Receptors 1 and 2
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Markedly Impaired Humoral Immune Response in Mice Deficient in Complement Receptors 1 and 2
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Journal Article
Markedly Impaired Humoral Immune Response in Mice Deficient in Complement Receptors 1 and 2
1996
Overview
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.
Publisher
National Academy of Sciences of the United States of America,National Acad Sciences,National Academy of Sciences
Subject
/ Antigens
/ Immunoglobulin G - biosynthesis
/ Immunoglobulin G - classification
/ Immunoglobulin M - biosynthesis
/ Isotypes
/ Mice
/ Receptors, Complement 3b - deficiency
/ Receptors, Complement 3b - genetics
/ Receptors, Complement 3d - deficiency
/ Receptors, Complement 3d - genetics
/ Rodents
/ Sheep
