Cell Reports· 2026Q1
Temporal CRAC channel blockade modulates the MYC-MXD axis to attenuate autoimmune inflammation
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- Q1SCImago
- 2026year
Short summary
Temporal blockade of CRAC channels disrupts Th17 cell effector functions and metabolic programming by altering the MYC-MXD axis, attenuating autoimmune inflammation in animal models and impacting human Th17 cells.
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Key points
- Temporal CRAC channel blockade impairs Th17 cell effector functions and metabolic programming.
- CRAC channel activity during differentiation maintains MYC function by repressing Mxd genes.
- Temporal CRAC channel block increases MXD expression, attenuating Th17 pathogenicity in an animal model of autoimmunity.
- The MYC-MXD axis regulation by CRAC channels extends to human Th17 cells, impacting cytokine production.
AI-generated from the title and abstract; the full text is not read.
Abstract
(CRAC) channels for their effector function. Here, we demonstrate that Th17 cells are uniquely sensitive to temporal inhibition of CRAC channels. Temporal CRAC channel block disturbed the effector functions and metabolic programming of Th17 cells, which were rescued by MYC expression. We uncovered a regulatory hierarchy in which CRAC channel activity during differentiation maintains MYC function by repressing Mxd genes, which antagonize MYC. In an animal model of autoimmunity, temporal CRAC channel block increased MXD expression to attenuate Th17 pathogenicity. These observations extend to human Th17 cells, where temporal CRAC channel blockade also impacts the MYC-MXD axis to impede cytokine production. Collectively, our study identifies a role for CRAC channels in regulating the MYC-MXD balance that governs Th17 effector function.
The authors' abstract, as published at the source. Cell Reports, 2026 · DOI ↗
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Field: Sensory Systems
Sensory SystemsNeuroscience