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)
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Infection and Immunity, 2006
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.
Infection and Immunity, 2008
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.
Delineation of the Function of a Major γδ T Cell Subset during Infection
Journal of Immunology, 2005
␥␦ T cells play important but poorly defined roles in pathogen-induced immune responses and in preventing chronic inflammation and pathology. A major obstacle to defining their function is establishing the degree of functional redundancy and heterogeneity among ␥␦ T cells. Using mice deficient in V␥1 ؉ T cells which are a major component of the ␥␦ T cell response to microbial infection, a specific immunoregulatory role for V␥1 ؉ T cells in macrophage and ␥␦ T cell homeostasis during infection has been established. By contrast, V␥1 ؉ T cells play no significant role in pathogen containment or eradication and cannot protect mice from immune-mediated pathology. Pathogen-elicited V␥1 ؉ T cells also display different functional characteristics at different stages of the host response to infection that involves unique and different populations of V␥1 ؉ T cells. These findings, therefore, identify distinct and nonoverlapping roles for ␥␦ T cell subsets in infection and establish the complexity and adaptability of a single population of ␥␦ T cells in the host response to infection that is not predetermined, but is, instead, shaped by environmental factors.
Delineation of the Function of a Major T Cell Subset during Infection
The Journal of Immunology, 2005
␥␦ T cells play important but poorly defined roles in pathogen-induced immune responses and in preventing chronic inflammation and pathology. A major obstacle to defining their function is establishing the degree of functional redundancy and heterogeneity among ␥␦ T cells. Using mice deficient in V␥1 ؉ T cells which are a major component of the ␥␦ T cell response to microbial infection, a specific immunoregulatory role for V␥1 ؉ T cells in macrophage and ␥␦ T cell homeostasis during infection has been established. By contrast, V␥1 ؉ T cells play no significant role in pathogen containment or eradication and cannot protect mice from immune-mediated pathology. Pathogen-elicited V␥1 ؉ T cells also display different functional characteristics at different stages of the host response to infection that involves unique and different populations of V␥1 ؉ T cells. These findings, therefore, identify distinct and nonoverlapping roles for ␥␦ T cell subsets in infection and establish the complexity and adaptability of a single population of ␥␦ T cells in the host response to infection that is not predetermined, but is, instead, shaped by environmental factors.
Infection {gamma}{delta} T Cell Subset during Delineation of the Function of a Major
2000
␥␦ T cells play important but poorly defined roles in pathogen-induced immune responses and in preventing chronic inflammation and pathology. A major obstacle to defining their function is establishing the degree of functional redundancy and heterogeneity among ␥␦ T cells. Using mice deficient in V␥1 ؉ T cells which are a major component of the ␥␦ T cell response to microbial infection, a specific immunoregulatory role for V␥1 ؉ T cells in macrophage and ␥␦ T cell homeostasis during infection has been established. By contrast, V␥1 ؉ T cells play no significant role in pathogen containment or eradication and cannot protect mice from immune-mediated pathology. Pathogen-elicited V␥1 ؉ T cells also display different functional characteristics at different stages of the host response to infection that involves unique and different populations of V␥1 ؉ T cells. These findings, therefore, identify distinct and nonoverlapping roles for ␥␦ T cell subsets in infection and establish the complexity and adaptability of a single population of ␥␦ T cells in the host response to infection that is not predetermined, but is, instead, shaped by environmental factors.
Epithelial defence by γδ T cells
… archives of allergy …, 2005
during intrathymic T cell development, there are only six expressed human V ␥ genes and a similarly small number of V ␦ genes . Nevertheless, the ␥␦ TCR repertoire can be at least as diverse as the ␣ TCR repertoire, due to the tremendous impact of mechanisms such as N nucleotide insertions during TCR gene rearrangement and usage of all three reading frames in the case of D ␦ elements . Interestingly, however, the expressed ␥␦ TCR repertoire is highly biased, resulting in a preferential expression of some V ␥ /V ␦ genes in certain anatomical localizations.
The role of γδ T lymphocytes in infection
Current Opinion in Immunology, 1991
Many recent studies suggest an involvement of y6 T ceils in the immune response to infectious pathogens including viruses, bacteria and eukaryotic parasites. However, it remains unclear whether the responses of ~6 T cells are specifically directed against antigens derived from these pathogens or against infection-induced, host-derived ligands.