No role of interleukin-4 in CD23/IgE-mediated enhancement of the murine antibody response in vivo.
Antigen-specific IgE up-regulates the specific IgM, IgG1, IgG2a and IgE response in vivo when given to mice together with antigen. The enhancement is mediated by the low-affinity receptor for IgE, Fc epsilon RII or CD23, as demonstrated both in CD23-deficient mice and by blocking CD23 with anti-CD23 monoclonal antibodies. A possible mechanism behind the regulatory effects of CD23 is that the IgE/ CD23/antigen complex is endocytosed by B cells, leading to increased antigen processing and presentation on major histocompatibility complex ( MHC) class II molecules to T helper cells. In the present study we have found that the expression of CD23 is reduced fivefold on splenic B cells in mice genetically deficient for IL-4. When IL-4-deficient mice and normal littermates were immunized with 2,4,6-trinitrophenyl (TNP)-specific IgE followed by bovine serum albumin (BSA)-TNP or with BSA-TNP alone, the BSA-specific IgG1 and IgG2a responses were equally well augmented by IgE in all mice. In addition, a low but significant IgE response was seen even in the IL-4-deficient mice. Thus, enhancement of the antibody response through IgE and CD23 occur in the absence of IL-4 and is not dependent on CD23 up-regulation.[1]References
- No role of interleukin-4 in CD23/IgE-mediated enhancement of the murine antibody response in vivo. Hjulström, S., Landin, A., Jansson, L., Holmdahl, R., Heyman, B. Eur. J. Immunol. (1995) [Pubmed]
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