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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. Cunhasubject
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 kinasedescription
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.
year | journal | country | edition | language |
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2019-04-05 | Journal of Experimental Medicine |