Mice deficient in CD23 reveal its modulatory role in IgE production but no role in T and B cell development.
To assess roles of CD23 in lymphocyte development and immune function in vivo, CD23-deficient mice ( CD23-/-) were generated. Mice heterozygous with respect to the defective allele ( CD23+/-) display 50% reduced levels of CD23 expression on CD23+ cell types. This pattern is consistent with a lack of parental or tissue-specific imprinting of the CD23 gene. Neither a 50% reduced level nor a complete lack of CD23 caused profound changes in lymphocyte compartments (thymocytes, peripheral T cells, and B-1 and B-2 B cells). The lack of CD23 also did not significantly alter in vitro the proliferative response of B cells triggered via the Ag receptor in combination with CD40 ligand, IL-2, and/or IL-4. Effects on polyclonal Ig production were tested in a Th2 cell-driven immune response in vivo after infection with Nippostrongylus brasiliensis, a parasite that dramatically enhances CD23 expression on B cells. In both primary and secondary immune responses, heterozygous CD23+/- mice developed slightly higher and CD23-/- mice similar serum IgE and IgG1 levels as compared with CD23+/+ (wild-type) mice. The increase in blood eosinophil counts was similar in all three types of mice. These findings show that after N. brasiliensis infection 1) a complete lack of CD23 in vivo neither prohibits nor significantly alters quantitatively polyclonal IgE levels in serum, and 2) a 50% reduction in cell-surface CD23 expression ( CD23+/- mice) correlates with slightly increased serum IgE levels.[1]References
- Mice deficient in CD23 reveal its modulatory role in IgE production but no role in T and B cell development. Stief, A., Texido, G., Sansig, G., Eibel, H., Le Gros, G., van der Putten, H. J. Immunol. (1994) [Pubmed]
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