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Andrew N. Macintyre
Researcher at Duke University
Publications - 44
Citations - 6480
Andrew N. Macintyre is an academic researcher from Duke University. The author has contributed to research in topics: T cell & Immune system. The author has an hindex of 20, co-authored 40 publications receiving 4893 citations. Previous affiliations of Andrew N. Macintyre include University of Dundee.
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Journal ArticleDOI
Cutting Edge: Distinct Glycolytic and Lipid Oxidative Metabolic Programs Are Essential for Effector and Regulatory CD4+ T Cell Subsets
Ryan D. Michalek,Valerie A. Gerriets,Sarah R. Jacobs,Andrew N. Macintyre,Nancie J. MacIver,Emily F. Mason,Sarah A. Sullivan,Amanda G. Nichols,Jeffrey C. Rathmell +8 more
TL;DR: Teff and Treg were selectively increased in Glut1 transgenic mice and reliant on glucose metabolism, whereas Treg had activated AMP-activated protein kinase and were dependent on lipid oxidation.
Journal ArticleDOI
Phosphoenolpyruvate Is a Metabolic Checkpoint of Anti-tumor T Cell Responses.
Ping-Chih Ho,Jessica D. Bihuniak,Andrew N. Macintyre,Matthew M. Staron,Xiaojing Liu,Robert A. Amezquita,Yao Chen Tsui,Yao Chen Tsui,Guoliang Cui,Goran Micevic,Jose C. Perales,Steven H. Kleinstein,E. Dale Abel,Karl L. Insogna,Stefan Feske,Jason W. Locasale,Marcus Bosenberg,Jeffrey C. Rathmell,Susan M. Kaech,Susan M. Kaech +19 more
TL;DR: New metabolic checkpoints for T cell activity are uncovered and it is demonstrated that metabolic reprogramming of tumor-reactive T cells can enhance anti-tumor T cell responses, illuminating new forms of immunotherapy.
Journal ArticleDOI
The glucose transporter Glut1 is selectively essential for CD4 T cell activation and effector function.
Andrew N. Macintyre,Valerie A. Gerriets,Amanda G. Nichols,Ryan D. Michalek,Michael C. Rudolph,Divino Deoliveira,Steven M. Anderson,E. Dale Abel,Benny J. Chen,Laura P. Hale,Jeffrey C. Rathmell +10 more
TL;DR: These data show a selective in vivo requirement for Glut1 in metabolic reprogramming of CD4 T cell activation and Teff expansion and survival and a selection of Treg cells that appeared functionally unaffected and able to suppress Teff, irrespective of Glut 1 expression.
Journal ArticleDOI
Metabolic Reprogramming of Macrophages GLUCOSE TRANSPORTER 1 (GLUT1)-MEDIATED GLUCOSE METABOLISM DRIVES A PROINFLAMMATORY PHENOTYPE
Alex J. Freemerman,Amy R. Johnson,Gina N. Sacks,J. Justin Milner,Erin L. Kirk,Melissa A. Troester,Andrew N. Macintyre,Pankuri Goraksha-Hicks,Jeffery C. Rathmell,Liza Makowski +9 more
TL;DR: It is reported that GLUT1 (SLC2A1) is the primary rate-limiting glucose transporter on proinflammatory-polarized MΦs, which may play an integral role in the promotion of obesity-associated insulin resistance.
Journal ArticleDOI
Metabolic programming and PDHK1 control CD4+ T cell subsets and inflammation
Valerie A. Gerriets,Rigel J. Kishton,Amanda G. Nichols,Andrew N. Macintyre,Makoto Inoue,Olga Ilkayeva,Peter S. Winter,Xiaojing Liu,Bhavana Priyadharshini,Marta E. Slawinska,Lea Haeberli,Catherine Huck,Laurence A. Turka,Kris C. Wood,Laura P. Hale,Paul Smith,Martin A. Schneider,Nancie J. MacIver,Jason W. Locasale,Christopher B. Newgard,Mari L. Shinohara,Jeffrey C. Rathmell +21 more
TL;DR: In this article, the authors evaluated CD4+ T cell populations in murine models and determined that inflammatory T cells maintain high expression of glycolytic genes, while Tregs are oxidative and require mitochondrial electron transport to proliferate and differentiate.