Journal article

ZBTB7B (Th-POK) Regulates the Development of IL-17-Producing CD1d-Restricted Mouse NKT Cells

Anselm Enders, Sanda Stankovic, Charis Teh, Adam P Uldrich, Mehmet Yabas, Torsten Juelich, John A Altin, Sandra Frankenreiter, Hannes Bergmann, Carla M Roots, Konstantinos Kyparissoudis, Chris C Goodnow, Dale I Godfrey

JOURNAL OF IMMUNOLOGY | AMER ASSOC IMMUNOLOGISTS | Published : 2012

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 inste..

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Grants

Awarded by National Institutes of Health


Awarded by Deutsche Forschungsgemeinschaft


Awarded by NHMRC


Awarded by NHMRC Australia


Awarded by NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES


Funding Acknowledgements

This work was supported by research grants from the Wellcome Trust, the National Institutes of Health (AI054523), the National Health and Medical Research Council of Australia (NHMRC), the CASS Foundation, and the Ramaciotti Foundations. A. E. was supported by a Deutsche Forschungsgemeinschaft Research Fellowship (EN 790/1-1) and an NHMRC Project Grant (APP1009190) and Career Development Fellowship (APP1035858). D. I. G. was supported by an NHMRC Senior Principal Research Fellowship (1020770). C. C. G. was supported by an NHMRC Australia Fellowship (585490) and by an Australian Research Council Federation Fellowship.

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