期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 102, 期 6, 页码 2010-2015出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0409449102
关键词
inflammatory bowel disease; G proteins; immune regulation; NKT cells; CD8 alpha alpha(+) T cells
资金
- NCI NIH HHS [CA-16042, P30 CA016042] Funding Source: Medline
- NIAID NIH HHS [AI-28697, P30 AI028697, F31 AI058919, AI058919] Funding Source: Medline
- NIDDK NIH HHS [DK69434, DK46763, R01 DK069434, DK19318, P01 DK046763] Funding Source: Medline
Inflammatory bowel disease reflects an aberrant mucosal CD4(+) T cell response to commensal enteric bacteria. In addition to regulatory T cell subsets, recent studies have revealed a protective role of B cells in murine CD4+ T cell colitis, but the relationship of their action to T cell immunoregulation is unknown. Here we report that mesenteric lymph node (MLN) B cells protect mice from colitis induced by Galphai2(-/-)CD4(+) T cells. Protection required the transfer of both B cells and CD8alpha(+) T cells; neither cell type alone was sufficient to inhibit CD4+ T cell-mediated colitis. Similar results were also observed in colitis induced by CD4(+)CD45RB(hi) T cells. Immunoregulation was associated with localization of B cells and expansion of CD4(-)CD8(-) CD3(+)NK1.1(+) T cells in the secondary lymphoid compartment, as well as expansion of CD4(+)CD8alpha(+) T cells in the intestinal intraepithelial compartment. MLN B cells from Galphai2(-/-) mice were deficient in a phenotypic subset and failed to provide cotransfer colitis protection. These findings indicate that protective action of B cells is a selective trait of MLN B cells acquired through a Galphai2-dependent developmental process and link B cells with the formation of regulatory T cells associated with mucosal immune homeostasis.
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