6533b7d0fe1ef96bd125a513

RESEARCH PRODUCT

PKM2 promotes Th17 cell differentiation and autoimmune inflammation by fine-tuning STAT3 activation

Marcos Henrique RosaMiriam M. FonsecaJuliana E Toller-kawahisaFernando Silva RamalhoDouglas Silva PradoGabriel Azevedo PublioTimna Varela MartinsLuis Eduardo Alves DamascenoFlávio P. VerasThiago M. CunhaAri WaismanJosé C. Alves-filhoFernando Q. Cunha

subject

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalCellular differentiationEncephalomyelitisPyruvate KinaseImmunologyFluorescent Antibody TechniqueAutoimmunityInflammationPKM2Real-Time Polymerase Chain ReactionArticleMice03 medical and health sciences0302 clinical medicineNeuroinflammationmedicineAnimalsImmunology and AllergySTAT3InflammationbiologyChemistryExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsFlow Cytometrymedicine.diseaseCell biologyMice Inbred C57BL030104 developmental biologyTumor progression030220 oncology & carcinogenesisbiology.proteinTh17 Cellsmedicine.symptomREAÇÃO EM CADEIA POR POLIMERASEPyruvate kinase

description

Th17 cells undergo metabolic reprogramming towards glycolysis to support their differentiation and pathogenicity. Damasceno et al. report that PKM2, a glycolytic enzyme, plays a nonmetabolic role in mediating Th17 cell differentiation and autoimmune neuroinflammation by fine-tuning STAT3 activation.

https://doi.org/10.1084/jem.20190613