1. CD8 T cells induce T-bet-dependent migration toward CXCR3 ligands by differentiated B cells produced during responses to alum-protein vaccines.
- Author
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Serre, Karine, Cunningham, Adam F., Coughlan, Ruth E., Lino, Andreia C., Rot, Antal, Hub, Elin, Moser, Katrin, Manz, Rudolf, Ferraro, Alastair, Bird, Roger, Toellner, Kai-Michael, Demengeot, Jocelyne, MacLennan, Ian C. M., and Mohr, Elodie
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T cells , *B cells , *LIGANDS (Biochemistry) , *CHEMOKINES , *INFLAMMATION - Abstract
Antibody-forming cells (AFCs) expressing the chemokine receptor CXCR3 are recruited to sites of inflammation where they help clear pathogens but may participate in autoimmune diseases. Here we identify a mechanism that induces CXCR3 expression by AFC and germinal center (GC) B cells. This happens when CD8 T cells are recruited into CD4 T cell-dependent B-cell responses. Ovalbumin-specific CD4 T cells (OTII) were trans ferred alone or with ovalbumin-specific CD6 T cells (OTI) and the response to subcutaneous alum-precipitated ovalbumin was followed in the draining lymph nodes. OTII cells alone Induce T helper 2-assoclated class switching to lgG1, but few AFC or GC B cells express CXCR3. By contrast, OTI-derived IFN-γ induces most responding GC B cells and AFCs to express high levels of CXCR3, and diverse switching to lgG2a, lgG2b, with some lgG1. Up-regulation of CXCR3 by GC B cells and AFCs and their migration toward Its ligand CXCL10 are shown to depend on B cells' intrinsic T-bet. a transcription factor downstream of the IFN-γR signaling. This model clarifies how precursors of long-lived AFCs and memory B cells acquire CXCR3 that causes their migration to inflammatory foci. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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