B Cell Developmental Requirement for the Gαi2 Gene

Mesenteric B cells centrally inhibit CD4+T cell colitis through interaction with regulatory T cell subsets

“…Alternatively, differentiation or activation of B cells in this compartment might include up-expression of cell-interaction molecules important for protective activity, such as CD1d and IL-10 (11). The present study demonstrates that formation of protective B cells requires G␣i2 genetic sufficiency, which is also required for the formation of B cell subsets important for bacterial immune surveillance (22). Phenotypically, these subsets include splenic MZ B cells and a MLN B cell subset with elevated CD19 and membrane IgM expression.…”

“…Native G␣i2 Ϫ/Ϫ mice on a 129 or a mixed B6͞129 background spontaneously develop colitis at the age of 6-8 weeks, a process that depends on Th1 CD4 ϩ T cell response and enteric microflora (22,24,(28)(29)(30). The model involves functional disorders in epithelial cells (31), professional antigen-presenting cells (32), B cells (22,33), and CD4 ϩ T cells (24,29,30,32), suggesting multiple requirements for G␣i2 in the formation of normal mucosal immunoregulation. To better define these roles, we have established a transfer model permitting separate evaluation of different G␣i2 Ϫ/Ϫ cell types in the development of colitis.…”

CD5 plays an inhibitory role in the suppressive function of murine CD4+ CD25+ Treg cells

“…B-1 B cells appear to suppress colitis since their absence in the Gαi2 knockout mice makes them susceptible to inflammatory bowel disease (61). Control of colitis by B cells has been proposed to be due to IL-10 secretion from B-1 cells (62).…”

Rig-I−/− mice develop colitis associated with downregulation of Gαi2

“…Heterotrimeric G proteins consist of α, β and γ subunits. Gαi2 is one of the Gα subunits, which has a role in a large variety of cellular and metabolic processes [19][20][21][22][23]. Furthermore, a decreased number of Peyer's patches was also observed in Gαi2 -/-mice [16,17,19].…”