Metabolic programming and PDHK1 control CD4+ T cell subsets and inflammation.

By Valerie A. Gerriets, Rigel J. Kishton, Amanda G. Nichols, Andrew N. Macintyre, M. Inoue, O. Ilkayeva, Peter S. Winter, Xiaojing Liu, Bhavana Priyadharshini, Marta Sławińska and 12 more. Journal of Clinical Investigation, 2015

664 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/bbd18639cc820746a9d5ef7bde8c5f7f698e52b9

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In Immunology

Citations in the corpus

From Krebs to Clinic: Glutamine Metabolism to Cancer Therapy (2016, neutral): “BPTES inhibition of hGA(124-551), a truncated form of human kidneytype glutaminase.”
Foxp3 reprograms T cell metabolism to function in low glucose high lactate environments (2017, background): “4 Cell Metabolism 25, 1–12, June 6, 2017 plex I inhibitor rotenone (Beier et al., 2015; Gerriets et al., 2015).”
Metabolic competition in the tumor microenvironment is a driver of cancer progression (2015, methodology): “Changes in glucose availability might also be reflected in changes in TIL OXPHOS.”
Mitochondria in the regulation of innate and adaptive immunity (2015, positive): “HIF-1 target PDHK1 is expressed in Th17 cells, but not in Treg cells, and diminishing PDHK1, the negative regulator of pyruvate dehydrogenase (PDH), suppressed Th17 formation and increased Treg formation in vitro (Gerriets et al., 2014).”