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COVER PICTURE: Absence of the splenic marginal zone in mice lacking the p110d subunit of phosphatidylinositol 3-kinase. Mutant mice lacking p110d reveal that this enzyme is responsible for the bulk of phosphatidylinositol 3,4,5-trisphosphate produced in response to B cell receptor (BCR) ligation. These mice have severely reduced B1 and marginal zone (MZ) B cell populations but apparently normal development of follicular B cells. p110d-deficient mice respond poorly to immunization with carbohydrate and protein antigens and fail to generate a germinal center reaction. P110d function is also required for BCR-mediated activation of Btk, PLCg2, and calcium flux. Immunofluorescent staining was performed on splenic cryosections using MOMA-1 (green) and anti-IgM (red) and revealed a marked reduction in MZ B cells in p110d2/2 mice (right panel). (See Wagner et al., p.805.)
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