Markedly impaired humoral immune response in mice deficient in complement receptors 1 and 2.
AUTOR(ES)
Molina, H
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=39612Documentos Relacionados
- Assessment of the humoral immune response against Plasmodium falciparum rhoptry-associated proteins 1 and 2.
- Impaired adrenal stress response in Toll-like receptor 2-deficient mice
- Inflammatory and immune responses are impaired in mice deficient in intercellular adhesion molecule 1.
- Impaired cardiac hypertrophic response in Calcineurin Aβ-deficient mice
- Saccharomyces uvarum mannoproteins stimulate a humoral immune response in mice