Identification of Novel [gamma][delta] T-Cell Subsets following Bacterial Infection in the Absence of V[gamma]1⁺ T Cells: Homeostatic Control of [gamma][delta] T-Cell Responses to Pathogen Infection by V[gamma]1⁺ T Cells (original) (raw)

Although ␥␦ T cells are a common feature of many pathogen-induced immune responses, the factors that influence, promote, or regulate the response of individual ␥␦ T-cell subsets to infection is unknown. Here we show that in the absence of V␥1 ؉ T cells, novel subsets of ␥␦ T cells, expressing T-cell receptor (TCR)-V␥ chains that normally define TCR␥␦ ؉ dendritic epidermal T cells (DETCs) (V␥5 ؉), intestinal intraepithelial lymphocytes (iIELs) (V␥7 ؉), and lymphocytes associated with the vaginal epithelia (V␥6 ؉), are recruited to the spleen in response to bacterial infection in TCR-V␥1 ؊/؊ mice. By comparison of phenotype and structure of TCR-V␥ chains and/or-V␦ chains expressed by these novel subsets with those of their epithelium-associated counterparts, the V␥6 ؉ T cells elicited in infected V␥1 ؊/؊ mice were shown to be identical to those found in the reproductive tract, from where they are presumably recruited in the absence of V␥1 ؉ T cells. By contrast, V␥5 ؉ and V␥7 ؉ T cells found in infected V␥1 ؊/؊ mice were distinct from V␥5 ؉ DETCs and V␥7 ؉ iIELs. Functional analyses of the novel ␥␦ T-cell subsets identified for infected V␥1 ؊/؊ mice showed that whereas the V␥5 ؉ and V␥7 ؉ subsets may compensate for the absence of V␥1 ؉ T cells by producing similar cytokines, they do not possess cytocidal activity and they cannot replace the macrophage homeostasis function of V␥1 ؉ T cells. Collectively, these findings identify novel subsets of ␥␦ T cells, the recruitment and activity of which is under the control of V␥1 ؉ T cells.