Defective antigen receptor-mediated proliferation of B and T cells in the absence of Vav

Article Abstract:

The vav gene present in the embryonic stem produces the Vav protein which affects the number of the T and B cells but no influence on their differentiation. Vav specifically affects the proliferation of the T and B cells controlled by antigen receptors and so antigen receptor-mediated signalling is reduced. Mutant mice, in which vav is absent, show a decrease in the number of T cells and the formation of interleukin 2 by the T cells. The number of most B cell types in these mutants is also less than the wild-type mice. However, the response of these mutants to stimuli independent of antigen receptors is unaffected.

T cells

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Defective T-cell receptor signalling and positive selection of Vav-deficient CD4+CD8+ thymocytes

Article Abstract:

The Vav protein is necessary for the proliferation of immature T and B lymphocytes and is involved in the signal transduction linked to lymphocytes antigen receptors which controls the maturation of the T cells. Chimeric mice embryos in which the embryonic stem cells containing a null vav gene are injected into blastocytes from mice deficient in recombinase activating gene-2 show a decrease in the maturation of the CD4+CD8+ thymocytes and the expression of the interleukin 2 receptor controlled by T cell receptor.

Antigen receptors, T cell, T cell antigen receptors, Lymphocytes

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Perinatal lethality and blocked B-cell development in mice lacking the tyrosine kinase Syk

Article Abstract:

Perinatal lethality and B cell development blockage occurs in the absence of the tyrosine kinase Syk, in mice. The kinase affects many physiological processes in mice. It plays an important role in embryogenesis by preventing hemorrhaging and in the differentiation of B-lineage cells. Syk signals the pre-B cell receptors to develop the mature B cells. The maturation of V-gamma-3+ thymocytes depends on Syk. The syk mutants are obtained by homologous recombination in embryonic stem cells.

Protein tyrosine kinase, Protein-tyrosine kinase, Lethal mutation

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