Id3 Restricts γδ NKT Cell Expansion by Controlling Egr2 and c-Myc Activity

The Journal of Immunology : Official Journal of the American Association of Immunologists
Baojun ZhangY Zhuang

Abstract

γδ NKT cells are neonatal-derived γδ T lymphocytes that are grouped together with invariant NKT cells based on their shared innate-like developmental program characterized by the transcription factor PLZF (promyelocytic leukemia zinc finger). Previous studies have demonstrated that the population size of γδ NKT cells is tightly controlled by Id3-mediated inhibition of E-protein activity in mice. However, how E proteins promote γδ NKT cell development and expansion remains to be determined. In this study, we report that the transcription factor Egr2, which also activates PLZF expression in invariant NKT cells, is essential for regulating γδ NKT cell expansion. We observed a higher expression of Egr family genes in γδ NKT cells compared with the conventional γδ T cell population. Loss of function of Id3 caused an expansion of γδ NKT cells, which is accompanied by further upregulation of Egr family genes as well as PLZF. Deletion of Egr2 in Id3-deficient γδ NKT cells prevented cell expansion and blocked PLZF upregulation. We further show that this Egr2-mediated γδ NKT cell expansion is dependent on c-Myc. c-Myc knockdown attenuated the proliferation of Id3-deficient γδ NKT cells, whereas c-Myc overexpression enhanced the prolifera...Continue Reading

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Citations

Aug 31, 2020·Journal of Cellular and Molecular Medicine·Lei LeiYaling Guo
Aug 6, 2019·Frontiers in Immunology·Konstantinos MengrelisTessa Crompton
Oct 16, 2020·Immunological Reviews·Michele K Anderson, Johanna S Selvaratnam

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