Stat5a/b are essential for normal lymphoid development and differentiation

Zhengju Yao(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Yongzhi Cui(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Wendy T. Watford(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Jay H. Bream(Johns Hopkins University), Kunihiro Yamaoka(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Bruce D. Hissong(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Denise Li(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Scott K. Durum(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Qiong Jiang(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Avinash Bhandoola(National Institute of Arthritis and Musculoskeletal and Skin Diseases), Lothar Hennighausen(National Institute of Arthritis and Musculoskeletal and Skin Diseases), John J. O’Shea(National Institute of Arthritis and Musculoskeletal and Skin Diseases)
Proceedings of the National Academy of Sciences
January 17, 2006
Cited by 379Open Access
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Abstract

Cytokines that use the common gamma chain gammac are critical for lymphoid development and function. Mutations of the IL-7 receptor, gammac, 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, gammac, and Jak3.


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