Journal
IMMUNITY
Volume 40, Issue 3, Pages 378-388Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2014.01.012
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Funding
- NIH NIAID Division of Intramural Research (DIR)
- NHLBI DIR
- Grants-in-Aid for Scientific Research [25893033] Funding Source: KAKEN
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Innate lymphoid cells (ILCs) are critical in innate immune responses to pathogens and lymphoid organ development. Similar to CD4(+) T helper (Th) cell subsets, ILC subsets positive for interleukin-7 receptor alpha (IL-7R alpha) produce distinct sets of effector cytokines. However, the molecular control of IL-7R alpha(+) ILC development and maintenance is unclear. Here, we report that GATA3 was indispensable for the development of all IL-7R alpha(+) ILC subsets and T cells but was not required for the development of classical natural killer cells. Conditionally Gata3-deficient mice had no lymph nodes and were susceptible to Citrobactor rodentium infection. After the ILCs had fully developed, GATA3 remained important for the maintenance and functions of ILC2s. Genome-wide gene expression analyses indicated that GATA3 regulated a similar set of cytokines and receptors in Th2 cells and ILC2s, but not in ILC3s. Thus, GATA3 plays parallel roles in regulating the development and functions of CD4(+) T cells and IL-7R alpha(+) ILCs.
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