| First Author | Menard LC | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 7 | Pages | 4857-66 |
| PubMed ID | 17878385 | Mgi Jnum | J:152333 |
| Mgi Id | MGI:4358023 | Doi | 10.4049/jimmunol.179.7.4857 |
| Citation | Menard LC, et al. (2007) B cells amplify IFN-gamma production by T cells via a TNF-alpha-mediated mechanism. J Immunol 179(7):4857-66 |
| abstractText | Aside from being the precursors of the Ab-secreting cells, B cells are engaged in other immune functions such as Ag presentation to T cells or cytokine production. These functions may contribute to the pathogenic role of B cells in a wide range of autoimmune diseases. We demonstrate that B cells acquire the capacity to amplify IFN-gamma production by CD4 and CD8 T cells during the course of the Th1 inflammatory response to Toxoplasma gondii infection. Using the two following different strategies, we observed that B cells from T. gondii-infected mice, but not from naive mice, induce higher IFN-gamma expression by splenic host T cells: 1) reconstitution of B cell-deficient mice with B cells expressing an alloantigen different from the recipients, and 2) adoptive transfer of B and T cells into RAG-/- mice. In vitro assays allowing the physical separation of T and B cells demonstrate that Ag-primed B cells enhance IFN-gamma production by T cells in a contact-dependent fashion. Using an OVA-transgenic strain of T. gondii and OVA-specific CD4 T cells, we observed that the proinflammatory effect of B cells is neither Ag specific nor requires MHCII expression. However, TNF-alpha expressed on the surface of B cells appears to mediate in part the up-regulation of IFN-gamma by the effector T cells. |
