NDLI: ZBTB7B (Th-POK) regulates the development of IL-17-producing CD1d-restricted mouse NKT cells.

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ZBTB7B (Th-POK) regulates the development of IL-17-producing CD1d-restricted mouse NKT cells.

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ZBTB7B (Th-POK) regulates the development of IL-17-producing CD1d-restricted mouse NKT cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Roots, Carla M. Teh, Charis Juelich, Torsten Stankovic, Sanda Frankenreiter, Sandra Bergmann, Hannes Goodnow, Chris C. Godfrey, Dale I. Kyparissoudis, Konstantinos Enders, Anselm Yabas, Mehmet Uldrich, Adam P. Altin, John A.
Description	Country affiliation: Australia Author Affiliation: Enders A ( Ramaciotti Immunization Genomics Laboratory, Department of Immunology, John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory 0200, Australia.)
Abstract	CD1d-dependent NKT cells represent a heterogeneous family of effector T cells including CD4(+)CD8(-) and CD4(-)CD8(-) subsets that respond to glycolipid Ags with rapid and potent cytokine production. NKT cell development is regulated by a unique combination of factors, however very little is known about factors that control the development of NKT subsets. In this study, we analyze a novel mouse strain (helpless) with a mis-sense mutation in the BTB-POZ domain of ZBTB7B and demonstrate that this mutation has dramatic, intrinsic effects on development of NKT cell subsets. Although NKT cell numbers are similar in Zbtb7b mutant mice, these cells are hyperproliferative and most lack CD4 and instead express CD8. Moreover, the majority of ZBTB7B mutant NKT cells in the thymus are retinoic acid-related orphan receptor Î³t positive, and a high frequency produce IL-17 while very few produce IFN-Î³ or other cytokines, sharply contrasting the profile of normal NKT cells. Mice heterozygous for the helpless mutation also have reduced numbers of CD4(+) NKT cells and increased production of IL-17 without an increase in CD8(+) cells, suggesting that ZBTB7B acts at multiple stages of NKT cell development. These results reveal ZBTB7B as a critical factor genetically predetermining the balance of effector subsets within the NKT cell population.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201486
Journal	The Journal of Immunology
Issue Number	11
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd1d Immunology Dna-binding Proteins Interleukin-17 Mutation, Missense Natural Killer T-cells Nuclear Receptor Subfamily 1, Group F, Member 3 Transcription Factors Animals Genetics Cd4-positive T-lymphocytes Metabolism Pathology Cd8-positive T-lymphocytes Cell Differentiation Cell Proliferation Gene Expression Interferon-gamma Biosynthesis Mice Mice, Transgenic Protein Structure, Tertiary T-lymphocyte Subsets Thymus Gland Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Zbtb7b (Th-POK) regulates the development of IL-17 producing CD1d-restricted mouse NKT-cells

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