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Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production
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Vasopressin receptor 1a-mediated negative regulation of B cell receptor signaling

Shuang-Bao Hu1, Zi-Shan Zhao, Christine Yhap

  • 1Clinical Neuroendocrinology Branch, National Institute of Mental Health, NIH, 10 Center Drive, 10/2D46, Bethesda, MD 20892, USA. sbh@codon.nih.gov

Journal of Neuroimmunology
|February 11, 2003
PubMed

We report here a study of T and B cell development and function in mice with disruption of the vasopressin receptor 1a (v1a) gene. Loss of the v1a receptor caused a shift from IgM(high)/IgD(high) to the more mature IgM(low)/IgD(high) B cells, a significantly greater extent of splenic B cells proliferation in response to anti-IgM stimulation, and enhanced IgG1 and IgG2b production in response to immune challenge with T-dependent antigen. B-1 cells were increased in v1a(-/-) mice. In contrast, T cell differentiation and activation were normal in v1a(-/-) mice. Our data identify a novel function for v1a in the periphery as a negative regulator of B cell receptor (BCR) signaling. These data suggest that in addition to its other stress-related effects, vasopressin may also serve as a counter-regulatory restraint upon the immune system during fight or flight situations.

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