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i2 Gene 1
* Department of Pathology and Laboratory Medicine and
Molecular Biology Institute, University of California, Los Angeles, CA 90095; and
Departments of Pediatrics and Immunology, University of Washington, Seattle, WA 98195
Null mutation of the G
i2 trimeric G protein results in a discrete and profound mucosal disorder, including inflammatory bowel disease (IBD), attenuation of IL-10 expression, and immune function polarized to Th1 activity. Genetic and adoptive transfer experiments have established a role for B cells and IL-10 in mucosal immunologic homeostasis and IBD resistance. In this study, we addressed the hypothesis that Gi2 is required for the development of IL-10-producing B cells. Gi2-/- mice were reduced in the relative abundance of marginal zone (MZ), transitional type 2 (T2), and B-1a B cells and significantly increased in follicular mature and B-1b B cells. Reconstitution of RAG2-/- mice with Gi2-/- bone marrow induced an IBD-like colitis and a deficiency in absolute numbers of MZ, T2, and B-1 B cells. Thus, the Gi2-/- genotype in colitis susceptibility and B cell development involved a cis effect within the hemopoietic compartment. In vitro, the B cell population of Gi2-/- mice was functionally deficient in LPS-induced proliferation and IL-10 production, consistent with the exclusive capacity of T2 and MZ cell subpopulations for LPS responsiveness. In vivo, Gi2-/- mice were selectively impaired for the IgM response to T-independent type II, consistent with the relative depletion of MZ and peritoneal B-1 subpopulations. Collectively, these results reveal a selective role for Gi2 in MZ and B-1 B cell development. Disorders of this Gi2-dependent process in B cell development may represent a mechanism for IBD susceptibility.
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