Article: article d'un périodique ou d'un magazine.
Selectively impaired development of intestinal T cell receptor gamma delta+ cells and liver CD4+ NK1+ T cell receptor alpha beta+ cells in T cell factor-1-deficient mice.
European Journal of Immunology
Date de publication
Publication types: Comparative Study ; Journal Article
T cell factor-1 (Tcf-1) is a transcription factor that binds to a sequence motif present in several T cell-specific enhancer elements. In Tcf-1-deficient (Tcf-1-/-) mice, thymocyte development is partially blocked at the transition from the CD4-8+ immature single-positive stage to the CD4+8+ double-positive stage, resulting in a marked decrease of mature peripheral T cells in lymph node and spleen. We report here that the development of most intestinal TCR gamma delta+ cells and liver CD4+ NK1.1+TCR alpha beta+ (NK1+T) cells, which are believed to be of extrathymic origin, is selectively impaired in Tcf-1-/- mice. In contrast, thymic and thymus-derived (splenic) TCR gamma delta+ cells are present in normal numbers in Tcf-1-/- mice, as are other T cell subsets in intestine and liver. Collectively, our data suggest that Tcf-1 is differentially required for the development of some extrathymic T cell subsets, including intestinal TCR gamma delta+ cells and liver CD4+ NK1+T cells.
Animals, Antigens, CD4, Cell Differentiation/immunology, DNA-Binding Proteins/genetics, Immunophenotyping, Intestinal Mucosa/cytology, Intestinal Mucosa/immunology, Intestine, Small/cytology, Intestine, Small/immunology, Killer Cells, Natural/cytology, Killer Cells, Natural/immunology, Liver/cytology, Liver/immunology, Lymphoid Enhancer-Binding Factor 1, Lymphopenia/genetics, Lymphopenia/immunology, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Receptors, Antigen, T-Cell, alpha-beta, Receptors, Antigen, T-Cell, gamma-delta, Spleen/cytology, Spleen/immunology, T Cell Transcription Factor 1, T-Lymphocyte Subsets/classification, T-Lymphocyte Subsets/cytology, Thymus Gland/cytology, Thymus Gland/immunology, Transcription Factors/deficiency, Transcription Factors/genetics
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