MICE DEFICIENT IN CD23 REVEAL ITS MODULATORY ROLE IN IGE PRODUCTION BUT NO ROLE IN T-CELL AND B-CELL DEVELOPMENT

To assess roles of CD23 in lymphocyte development and immune function in vivo, CD23-deficient mice (CD23(-/-)) were generated. Mice heterozy gous with respect to the defective allele (CD23(+/-)) display 50% redu ced levels of CD23 expression on CD23(+) cell types. This pattern is c onsistent with a lack of parental or tissue-specific imprinting of the CD23 gene. Neither a 50% reduced level nor a complete lack of CD23 ca used profound changes in lymphocyte compartments (thymocytes, peripher al T cells, and B-1 and B-2 B cells). The lack of CD23 also did not si gnificantly alter in vitro the proliferative response of B cells trigg ered 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-d riven immune response in vivo after infection with Nippostrongylus bra siliensis, a parasite that dramatically enhances CD23 expression on B cells. In both primary and secondary immune responses, heterozygous CD 23(+/-) mice developed slightly higher and CD23(-/-) mice similar seru m 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 c omplete lack of CD23 in vivo neither prohibits nor significantly alter s quantitatively polyclonal IgE levels in serum, and 2) a 50% reductio n in cell-surface CD23 expression (CD23(+/-) mice) correlates with sli ghtly increased serum IgE levels.