Alister C. Ward's The Jak-Stat Pathway in Hematopoiesis (Molecular Biology PDF

By Alister C. Ward

ISBN-10: 1587060744

ISBN-13: 9781587060748

ISBN-10: 1587061147

ISBN-13: 9781587061141

This publication for the 1st time comprehensively surveys the examine investigating the Jak-Stat pathway and its function in common blood improvement in addition to its perturbation in sickness. It attracts at the services of world-renowned scientific researchers to take the reader from easy biology via to contemporary healing advances.

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Extra info for The Jak-Stat Pathway in Hematopoiesis (Molecular Biology Intelligence Unit, 20)

Example text

In support of this model is evidence from TCR transgenic mice showing that the aberrant expansion of mature Jak3-/- T cells is antigen-dependent. 10 (ovalbumin peptide-specific) transgenic TCR contain cells that express the Tg receptor that can be identified with an anti-clonotypic antibody, and a subset of T cells expressing endogenous T ell receptors. 10 TCR have a surface phenotype characterisitic of naïve, quiescent T lymphocytes. 167 This strongly suggests that there is an imbalance between antigen-driven proliferative signals and negative regulatory mechanisms which results in the accumulation of high levels of activated peripheral T cells in he Jak3-deficient mice.

10 TCR have a surface phenotype characterisitic of naïve, quiescent T lymphocytes. 167 This strongly suggests that there is an imbalance between antigen-driven proliferative signals and negative regulatory mechanisms which results in the accumulation of high levels of activated peripheral T cells in he Jak3-deficient mice. 167 Surprisingly, although Jak3-/CD4+ T cells incorporate markedly enhaned levels of BrdU in vivo, suggesting a very high level of proliferation, hese cells are refractory to all polyclonal stimuli tested in vitro.

All of the mutations result in the accumulation of mature, CD4+ T cells with an activated/memory surface phenotype. Due to the peiotropic effects of Jak3 deficiency on proliferation and signal transduction through multiple receptors, and reduced T and B cell development, Jak3-/- or #c-/- T cells do not induce severe autoimmune disorders. In contrast, IL-2 deficiency results in the loss f a single signaling pathway that is critical for negative regulation of immune responses, while all other Jak3-dependent signaling complexes remain intact.

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The Jak-Stat Pathway in Hematopoiesis (Molecular Biology Intelligence Unit, 20) by Alister C. Ward


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