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

A Enders; S Stankovic; C Teh; AP Uldrich; M Yabas; T Juelich; JA Altin; S Frankenreiter; H Bergmann; CM Roots; K Kyparissoudis; CC Goodnow; DI Godfrey

Journal article

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

A Enders, S Stankovic, C Teh, AP Uldrich, M Yabas, T Juelich, JA Altin, S Frankenreiter, H Bergmann, CM Roots, K Kyparissoudis, CC Goodnow, DI Godfrey

Journal of Immunology | AMER ASSOC IMMUNOLOGISTS | Published : 2012

DOI: 10.4049/jimmunol.1201486

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 expr..

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University of Melbourne Researchers

Charis En-Yi Teh Author

Adam Uldrich Author

Dale Godfrey Author

Related Projects (3)

IMMUNE REGULATION EFFECTOR FUNCTION AND THERAPY

We seek to understand how white blood cells detect and destroy disease, and how molecules of the immune system punch holes in diseased cells..

IMMUNE REGULATION EFFECTOR FUNCTION AND THERAPY

We seek to understand how white blood cells detect and destroy disease, and how molecules of the immune system punch holes in diseased cells..

RESEARCH FELLOWSHIP

Professor Godfrey is an immunologist with a long standing history as a pioneer in the study of a specialised type of white blood cell, known..

Grants

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.