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  Genetic Evidence for an Evolutionarily Conserved Role of IL-7 Signaling in T Cell Development of Zebrafish

Iwanami, N., Mateos, F., Hess, I., Riffel, N., Soza-Ried, C., Schorpp, M., et al. (2011). Genetic Evidence for an Evolutionarily Conserved Role of IL-7 Signaling in T Cell Development of Zebrafish. The Jounal of Immunology, 186, 7060-7066.

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 Creators:
Iwanami, Norimasa1, Author           
Mateos, Fernando1, Author           
Hess, Isabell1, Author           
Riffel, Nico1, Author           
Soza-Ried, Cristian2, Author           
Schorpp, Michael1, Author           
Boehm, Thomas1, Author           
Affiliations:
1Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
2Department of Developmental Biology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243650              

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 Abstract: In mammals, the cytokine IL-7 is a key regulator of various aspects of lymphocyte differentiation and homeostasis. Because of the difficulty of identifying cytokine homologs in lower vertebrates and the paucity of assay systems and reagents, the degree of functional conservation of cytokine signaling pathways, particularly those pertaining to lymphocyte development, is unclear. In this article, we report on the analysis and characterization of three zebrafish mutants with severely impaired thymopoiesis. The identification of affected genes by positional cloning revealed components of the IL-7 signaling pathway. A presumptive null allele of the zebrafish homolog of the IL-7Rα-chain causes substantially reduced cellularity of the thymus but spares B cell development in the kidney. Likewise, nonsense mutations in the zebrafish homologs of janus kinases JAK1 and JAK3 preferentially affect T cell development. The functional interactions of the cytokine receptor components were examined in the three groups of fish hetero- or homozygous for either il7r and jak1, il7r and jak3, or jak1 and jak3 mutations. The differential effects on T cell development arising from the different genotypes could be explained on the basis of the known structure of the mammalian IL-7R complex. Because IL-7 signaling appears to be a universal requirement for T cell development in vertebrates, the mutants described in this article represent alternative animal models of human immunodeficiency syndromes amenable to large-scale genetic and chemical screens.

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Language(s): eng - English
 Dates: 2011
 Publication Status: Issued
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 Rev. Type: Peer
 Identifiers: eDoc: 577339
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Title: The Jounal of Immunology
  Alternative Title : J. Immunol.
Source Genre: Journal
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Pages: - Volume / Issue: 186 Sequence Number: - Start / End Page: 7060 - 7066 Identifier: -