Journal article

A reporter mouse reveals lineage-specific and heterogeneous expression of IRF8 during lymphoid and myeloid cell differentiation

H Wang, M Yan, J Sun, S Jain, R Yoshimi, SM Abolfath, K Ozato, WG Coleman, AP Ng, D Metcalf, L DiRago, SL Nutt, HC Morse

Journal of Immunology | Published : 2014

Abstract

The IFN regulatory factor family member 8 (IRF8) regulates differentiation of lymphoid and myeloid lineage cells by promoting or suppressing lineage-specific genes. How IRF8 promotes hematopoietic progenitors to commit to one lineage while preventing the development of alternative lineages is not known. In this study, we report an IRF8-EGFP fusion protein reporter mouse that revealed previously unrecognized patterns of IRF8 expression. Differentiation of hematopoietic stem cells into oligopotent progenitors is associated with progressive increases in IRF8-EGFP expression. However, significant induction of IRF8-EGFP is found in granulocyte-myeloid progenitors and the common lymphoid progenito..

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University of Melbourne Researchers

Grants

Awarded by National Institute of Child Health and Human Development


Funding Acknowledgements

This work was supported by the Intramural Research Program of the National Institutes of Health's National Institute of Allergy and Infectious Diseases (to H.W., J.S., S.J., S.M.A., and H.C.M.), the National Institute of Child Health and Human Development (to R.Y. and K.O.), and the National Institute of Diabetes and Digestive and Kidney Diseases (to M.Y. and W.G.C.). A.P.N., L.D., and D.M. were supported by Program Grant 1016647 and Independent Research Institutes Infrastructure Support Scheme Grant 361646 from the Australian National Health and Medical Research Council. This work was also supported by the Carden fellowship (to D.M.) from the Cancer Council of Victoria, a Cure Cancer Australia/Leukaemia Foundation Australia postdoctoral fellowship and a Lions fellowship from the Cancer Council of Victoria (to A.P.N.), and the Victorian State Government Operational Infrastructure. S.L.N. was supported by an Australian Research Council Future fellowship.