Transcription factor p73 regulates Th1 differentiation

Min Ren, Majid Kazemian, Ming Zheng, JianPing He, Peng Li, Jangsuk Oh, Wei Liao, Jessica Li, Jonathan Rajaseelan, Brian L. Kelsall, Gary Peltz and Warren J. Leonard ()
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Min Ren: National Heart, Lung, and Blood Institute
Majid Kazemian: National Heart, Lung, and Blood Institute
Ming Zheng: Stanford University School of Medicine
JianPing He: National Institute of Allergy and Infectious Diseases
Peng Li: National Heart, Lung, and Blood Institute
Jangsuk Oh: National Heart, Lung, and Blood Institute
Wei Liao: National Heart, Lung, and Blood Institute
Jessica Li: National Heart, Lung, and Blood Institute
Jonathan Rajaseelan: National Heart, Lung, and Blood Institute
Brian L. Kelsall: National Institute of Allergy and Infectious Diseases
Gary Peltz: Stanford University School of Medicine
Warren J. Leonard: National Heart, Lung, and Blood Institute

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract Inter-individual differences in T helper (Th) cell responses affect susceptibility to infectious, allergic and autoimmune diseases. To identify factors contributing to these response differences, here we analyze in vitro differentiated Th1 cells from 16 inbred mouse strains. Haplotype-based computational genetic analysis indicates that the p53 family protein, p73, affects Th1 differentiation. In cells differentiated under Th1 conditions in vitro, p73 negatively regulates IFNγ production. p73 binds within, or upstream of, and modulates the expression of Th1 differentiation-related genes such as Ifng and Il12rb2. Furthermore, in mouse experimental autoimmune encephalitis, p73-deficient mice have increased IFNγ production and less disease severity, whereas in an adoptive transfer model of inflammatory bowel disease, transfer of p73-deficient naïve CD4+ T cells increases Th1 responses and augments disease severity. Our results thus identify p73 as a negative regulator of the Th1 immune response, suggesting that p73 dysregulation may contribute to susceptibility to autoimmune disease.

Date: 2020
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DOI: 10.1038/s41467-020-15172-5

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