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STIM1-mediated NFAT signaling synergizes with STAT1 to control T-bet expression and T H 1 differentiation
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STIM1-mediated NFAT signaling synergizes with STAT1 to control T-bet expression and T H 1 differentiation
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Journal Article
STIM1-mediated NFAT signaling synergizes with STAT1 to control T-bet expression and T H 1 differentiation
2025
Overview
Stromal interaction molecule 1 (STIM1) is critical for store-operated Ca
entry (SOCE) and T cell activation. T helper 1 (T
1) cells, which express T-bet (encoded by TBX21), mediate immunity to intracellular pathogens. Although SOCE is known to regulate other T
lineages, its role in Th1 differentiation remains unclear. Here, we report a patient with an intronic loss-of-function mutation in STIM1, which abolishes SOCE and causes immunodeficiency. We demonstrate that SOCE promotes nuclear factor of activated T cells (NFAT) binding to conserved noncoding sequence (CNS)-12 in the TBX21 enhancer and enables NFAT to synergize with STAT1 to mediate TBX21 expression. While SOCE-deficient CD4
T cells have reduced expression of TBX21 in the absence of interleukin-12 (IL-12), their expression of IL-12 receptors β1 and β2 is increased, sensitizing them to IL-12 signaling and allowing IL-12 to rescue T-bet expression. Our study reveals that the STIM1-SOCE-NFAT signaling axis is essential for the differentiation of Th1 cells depending on the cytokine milieu.
Subject
/ Cell Differentiation - genetics
/ Cell Differentiation - immunology
/ Humans
/ Mice
/ Neoplasm Proteins - genetics
/ Neoplasm Proteins - metabolism
/ NFATC Transcription Factors - metabolism
/ Signal Transduction - immunology
/ STAT1 Transcription Factor - genetics
/ STAT1 Transcription Factor - metabolism
/ Stromal Interaction Molecule 1 - genetics
/ Stromal Interaction Molecule 1 - metabolism
/ T-Box Domain Proteins - genetics
