Identification of novel γδ T-cell subsets following bacterial infection in the absence of Vγ1+ T cells: Homeostatic control of γδ T-cell responses to pathogen infection by Vγ1 + T cells

Although γδ T cells are a common feature of many pathogen-induced immune responses, the factors that influence, promote, or regulate the response of individual γδ T-cell subsets to infection is unknown. Here we show that in the absence of Vγ1+ T cells, novel subsets of γδ T cells, expressing T-cell receptor (TCR)-Vγ chains that normally define TCRγδ+ dendritic epidermal T cells (DETCs) (Vγ5+), intestinal intraepithelial lymphocytes (iIELs) (Vγ7+), and lymphocytes associated with the vaginal epithelia (Vγ6+), are recruited to the spleen in response to bacterial infection in TCR-Vγ1-/- mice. By comparison of phenotype and structure of TCR-Vγ chains and/or -Vδ chains expressed by these novel subsets with those of their epithelium-associated counterparts, the Vγ6+ T cells elicited in infected Vγ1-/- mice were shown to be identical to those found in the reproductive tract, from where they are presumably recruited in the absence of Vγ1+ T cells. By contrast, Vγ5+ and Vγ7+ T cells found in infected Vγ1-/- mice were distinct from Vγ5+ DETCs and Vγ7+ iIELs. Functional analyses of the novel γδ T-cell subsets identified for infected Vγ1-/- mice showed that whereas the Vγ5 + and Vγ7+ subsets may compensate for the absence of Vγ1+ T cells by producing similar cytokines, they do not possess cytocidal activity and they cannot replace the macrophage homeostasis function of Vγ1+ T cells. Collectively, these findings identify novel subsets of γδ T cells, the recruitment and activity of which is under the control of Vγ1+ T cells. Copyright © 2006, American Society for Microbiology. All Rights Reserved.