Impaired IL-12 responses and enhanced development of Th2 cells in Stat4-deficient mice

Article Abstract:

An insertional mutation in the signal transducer and activator of transcription 4 (Stat4) gene produces defects in the response of the cells to interleukin (IL) 12 and increases the level of the Th2 cells. The mutant cells show no interferon-gamma secretion in response to activation of T cells by IL-12. The mutants also show no T cell proliferation, Th1 differentiation and cytotoxicity of natural killer cells in response to IL-12. A study indicates that the protein is essential for IL-12-mediated processes in lymphocytes, and Th1 and Th2 differentiation.

Research, Cell differentiation

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Requirement for Stat4 in interleukin-12-mediated responses of natural killer and T cells

Article Abstract:

The signal transducer and activator of transcription 4 (Stat4) is essential for the activity, controlled by interleukin (IL) 12, of natural killers (NK) and T cells. Mice with an insertional mutation in the Stat4 gene produce no interferon-gamma and the activity of NK cells against its target cells is absent. The mutants show defects in IL-12 activated proliferation of lymphocytes and differentiation of Th1 helper T cells. However, the mice are viable and show normal spermatogenesis, haematopoiesis and serum levels of immunoglobulin isotypes.

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Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene

Article Abstract:

A lack of the signal transducer and activator of transcription 6 (Stat6) gene in mice affects the expression of cell surface markers, differentiation of Th2 helper T-cells, and immunoglobulin class switching to IgE. The absence of Stat6 affects IL-4 mediated functions while the lymphoid cell development is unaffected. IL-4-induced cell proliferation is only slightly affected. However, the mutant mice are viable and exhibit normal development.

Mutation (Biology), Mutation, Interleukin-4

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