Journal
NATURE IMMUNOLOGY
Volume 10, Issue 8, Pages 872-U98Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1747
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Funding
- NIAID NIH HHS [R01 AI048636, R01 AI048636-05, R56 AI048636, AI048636] Funding Source: Medline
- Grants-in-Aid for Scientific Research [21790334] Funding Source: KAKEN
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T helper type 2 (T(H)2) bias, which is the propensity of naive CD4(+) T cells to differentiate into interleukin 4 (IL-4)-secreting T(H)2 cells, is a genetic trait that affects susceptibility to infectious, autoimmune and allergic diseases. T(H)2 bias correlates with the amount of IL-4 initially secreted by newly activated helper T cells that feeds back positively through the pathway of the IL-4 receptor and the transcription factors STAT6 and GATA-3 to drive T(H)2 development. Here we identify Mina, a member of the jumonji C (JmjC) protein family, as a genetic determinant of T(H)2 bias. Mina specifically bound to and repressed the Il4 promoter. Mina overexpression in transgenic mice impaired Il4 expression, whereas its knockdown in primary CD4(+) T cells led to Il4 derepression. Our findings collectively provide mechanistic insight into an Il4-regulatory pathway that controls helper T cell differentiation and genetic variation in T(H)2 bias.
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