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      Bcl11b is required for differentiation and survival of alphabeta T lymphocytes.

      Nature immunology

      immunology, ras Proteins, genetics, Zinc Fingers, cytology, Thymus Gland, T-Lymphocytes, Receptors, Antigen, T-Cell, gamma-delta, Mice, SCID, Mice, Knockout, Mice, Inbred BALB C, Mice, Male, Lymphopoiesis, In Situ Nick-End Labeling, Hematopoietic Stem Cells, Female, Cell Differentiation, Apoptosis, Animals, Newborn, Animals

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          Abstract

          The gene Bcl11b, which encodes zinc finger proteins, and its paralog, Bcl11a, are associated with immune-system malignancies. We have generated Bcl11b-deficient mice that show a block at the CD4-CD8- double-negative stage of thymocyte development without any impairment in cells of B- or gammadelta T cell lineages. The Bcl11b-/- thymocytes showed unsuccessful recombination of V(beta) to D(beta) and lacked the pre-T cell receptor (TCR) complex on the cell surface, owing to the absence of Tcrb mRNA expression. In addition, we saw profound apoptosis in the thymus of neonatal Bcl11b-/- mice. These results suggest that Bcl11b is a key regulator of both differentiation and survival during thymocyte development.

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          Journal
          10.1038/ni927
          12717433

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