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The absence of IgE antibody-mediated augmentation of immune responses in CD23-deficient mice
H Fujiwara1, H Kikutani, S Suematsu
1Research Institute, Osaka Medical Center for Maternal and Child Health, Japan.
Insights
Mice lacking the CD23 antigen, a receptor for IgE, showed normal immune responses. However, IgE-mediated enhancement of antibody production was significantly impaired in these CD23-deficient mice.
Area of Science:
- Immunology
- Molecular Biology
Background:
- CD23 (Fc epsilon RII) is a low-affinity IgE receptor on B cells with diverse proposed functions.
- In vivo roles of CD23 remain unclear despite ascribed functions like IgE regulation and B-cell growth promotion.
Purpose of the Study:
- To investigate the in vivo functions of CD23.
- To elucidate the role of CD23 in immune responses using genetically modified mice.
Main Methods:
- Generation and analysis of CD23-deficient mice.
- Assessment of lymphocyte differentiation and antibody responses (including IgE) after immunization and infection.
- Evaluation of germinal center formation and B-cell proliferation in vitro.
Main Results:
- CD23-deficient mice exhibited normal lymphocyte development and antibody production, including IgE responses.
- Germinal center formation and B-cell proliferation were unaffected in the absence of CD23.
- A severe impairment in antigen-specific IgE-mediated enhancement of antibody responses was observed.
Conclusions:
- CD23 is not essential for basic lymphocyte differentiation or general antibody production.
- The primary in vivo role of CD23 appears to be the enhancement of IgE-mediated antibody responses.
Abstract:
The CD23 antigen, a low-affinity receptor for IgE (Fc epsilon RII), is a type II membrane-bound glycoprotein expressed on various cells, particularly mature B cells. A number of functions have been ascribed to CD23, including specific regulation of IgE production, IgE-mediated cytotoxicity and release of mediators, IgE-dependent antigen focusing, promotion of B-cell growth, prevention of germinal center B cells from apoptosis, proliferation of myeloid precursors, and maturation of early thymocytes. It is not clear whether these activities represent in vivo functions. To explore in vivo functions of CD23, we have produced CD23-deficient mice. These mice displayed normal lymphocyte differentiation and could mount normal antibody responses, including IgE responses upon immunization with T-dependent antigens and infection with Nippostrongyrus brasiliensis. Germinal center formation after immunization and in vitro proliferative response of B cells were not affected in mutant mice. However, antigen-specific IgE-mediated enhancement of antibody responses was severely impaired.
