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Stat5a/b are essential for normal lymphoid development and differentiation

  1. Author:
    Yao, Z. J.
    Cui, Y. Z.
    Watford, W. T.
    Bream, J. H.
    Yamaoka, K.
    Hissong, B. D.
    Li, D.
    Durum, S. K.
    Jiang, Q. O.
    Bhandoola, A.
    Hennighausen, L.
    O'Shea, J. J.

  2. Author Address

    NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA. NIDDKD, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA. NCI, Mol Immunoregulat Lab, Frederick, MD 21702 USA. Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA O'Shea, JJ, NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bldg 10,Room 9N262,10 Ctr Dr,MSC-1820, Bethesda, MD 20892 USA
    1. Year: 2006
    2. Date: JAN 24
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 103
    2. 4
    3. Pages: 1000-1005
  4. Type of Article: Article
  1. Abstract:

    Cytokines that use the common gamma chain gamma c are critical for lymphoid development and function. Mutations of the IL-7 receptor, gamma c, or its associated kinase, Jak3, are the major cause of human severe combined immunodeficiency. Although activated by IL-7, Stat5a/b (Stat, signal transducer and activator of transcription) have been thought to play limited roles in lymphoid development. However, we now show that mice completely deficient in Stat5a/b have severely impaired lymphoid development and differentiation. Absence of Stat5 also abrogates T cell receptor gamma rearrangement and survival of peripheral CD8(+) T cells. Thus, deficiency of Stat5 results in severe combined immunodeficiency, similar in many respects to deficiency of IL-7R, gamma c, and Jak3

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External Sources

  1. View record in Web of Science®
  2. WOS: 000234938300031

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