Journal
JOURNAL OF IMMUNOLOGY
Volume 196, Issue 5, Pages 2015-2019Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1501841
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Funding
- National Institutes of Health [R01AI 109842, AI40127, R01AI072543, U19 AI109976]
- Jane Coffin Childs Memorial Fund
- Pew Latin American Fellows Program in the Biomedical Sciences
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Follicular CD4(+) Th (Tfh) cells provide B cell help in germinal center reactions that support class switching, somatic hypermutation, and the generation of high-affinity Abs. In this article, we show that deficiency in NFAT1 and NFAT2 in CD4(+) T cells leads to impaired germinal center reactions upon viral infection because of reduced Tfh cell differentiation and defective expression of proteins involved in T/B interactions and B cell help, including ICOS, PD-1, and SLAM family receptors. Genome-wide chromatin immunoprecipitation data suggest that NFAT proteins likely directly participate in regulation of genes important for Tfh cell differentiation and function. NFAT proteins are important TCR and Ca2+-dependent regulators of T cell biology, and in this article we demonstrate a major positive role of NFAT family members in Tfh differentiation.
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