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Title: Activins and inhibins: Novel regulators of thymocyte development

Journal Article · · Biochemical and Biophysical Research Communications
;  [1];  [2];  [3];  [1];  [4];  [5];  [1]
  1. Departamento de Inmunologia, Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico, Circuito Escolar s/n, Mexico, DF 04510 (Mexico)
  2. Departamento de Medicina Genomica y Toxicologia Ambiental, Instituto de Investigaciones Biomedicas, UNAM, Mexico, DF (Mexico)
  3. Departmento de Biologia Celular, Instituto de Fisiologia Celular, UNAM, Mexico, DF (Mexico)
  4. Departments of Pathology, Molecular and Cellular Biology, and Molecular and Human Genetics, Baylor College of Medicine, Houston, TX (United States)
  5. Departamento de Biologia Celular y Tisular, Facultad de Medicina, UNAM, Mexico, DF (Mexico)

Activins and inhibins are members of the transforming growth factor-{beta} superfamily that act on different cell types and regulate a broad range of cellular processes including proliferation, differentiation, and apoptosis. Here, we provide the first evidence that activins and inhibins regulate specific checkpoints during thymocyte development. We demonstrate that both activin A and inhibin A promote the DN3-DN4 transition in vitro, although they differentially control the transition to the DP stage. Whereas activin A induces the accumulation of a CD8{sup +}CD24{sup hi}TCR{beta}{sup lo} intermediate subpopulation, inhibin A promotes the differentiation of DN4 to DP. In addition, both activin A and inhibin A appear to promote CD8{sup +}SP differentiation. Moreover, inhibin {alpha} null mice have delayed in vitro T cell development, showing both a decrease in the DN-DP transition and reduced thymocyte numbers, further supporting a role for inhibins in the control of developmental signals taking place during T cell differentiation in vivo.

OSTI ID:
21255957
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 381, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2009.02.029; PII: S0006-291X(09)00282-4; Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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