Ryan Kyle
Max Planck Society
25 Papers
3 Citations
Ryan Kyle is an academic researcher from Max Planck Society. The author has contributed to research in topics: Immune system & Biology. The author has an hindex of 15, co-authored 21 publications. Previous affiliations of Ryan Kyle include Malaghan Institute of Medical Research.
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Papers
Unraveling the Complex Interplay Between T Cell Metabolism and Function
TL;DR: How T cell metabolism can have profound effects on health and disease and where it might be a promising target to treat a variety of pathologies is discussed.
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Cutaneous immunosurveillance and regulation of inflammation by group 2 innate lymphoid cells
Ben Roediger,Ryan Kyle,Kwok Ho Yip,Nital Sumaria,Nital Sumaria,Thomas V. Guy,Brian S. Kim,Andrew J. Mitchell,Szun S. Tay,Rohit Jain,Elizabeth Forbes-Blom,Xi Chen,Philip L. Tong,Philip L. Tong,Philip L. Tong,Holly A. Bolton,David Artis,William E. Paul,Barbara Fazekas de St Groth,Barbara Fazekas de St Groth,Michele A. Grimbaldeston,Graham Le Gros,Wolfgang Weninger,Wolfgang Weninger,Wolfgang Weninger +24 more
TL;DR: The data show that ILC2 cells have both pro- and anti-inflammatory properties and identify a previously unknown interactive pathway between two innate populations of cells of the immune system linked to type 2 immunity and allergic diseases.
Mitochondrial Integrity Regulated by Lipid Metabolism Is a Cell-Intrinsic Checkpoint for Treg Suppressive Function
Cameron S. Field,Francesc Baixauli,Ryan Kyle,Daniel J. Puleston,Alanna M. Cameron,David E. Sanin,Keli L. Hippen,Michael Loschi,Govindarajan Thangavelu,Mauro Corrado,Joy Edwards-Hicks,Katarzyna M. Grzes,Edward J. Pearce,Bruce R. Blazar,Erika L. Pearce +14 more
TL;DR: It is shown that in Tregs, genetic or pharmacologic inhibition of FABP5 function causes mitochondrial changes underscored by decreased OXPHOS, impaired lipid metabolism, and loss of cristae structure that underlie enhanced immunosuppression in the tumor microenvironment.
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Acetate Promotes T Cell Effector Function during Glucose Restriction
Jing Qiu,Matteo Villa,David E. Sanin,Michael D. Buck,David O’Sullivan,Reagan W. Ching,Mai Matsushita,Katarzyna M. Grzes,Frances Winkler,Chih-Hao Chang,Jonathan D. Curtis,Ryan Kyle,Nikki van Teijlingen Bakker,Mauro Corrado,Fabian Haessler,Francesca Alfei,Joy Edwards-Hicks,Leonard B. Maggi,Dietmar Zehn,Takeshi Egawa,Bertram Bengsch,Ramon I. Klein Geltink,Thomas Jenuwein,Edward J. Pearce,Edward J. Pearce,Erika L. Pearce +25 more
TL;DR: Hyporesponsive T cells can be epigenetically remodeled and reactivated by acetate, suggesting that pathways regulating the use of substrates alternative to glucose could be therapeutically targeted to promote T cell function during cancer.
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Mitochondrial Priming by CD28
Ramon I. Klein Geltink,David O’Sullivan,Mauro Corrado,Anna Bremser,Michael D. Buck,Joerg M. Buescher,Elke Firat,Xuekai Zhu,Gabriele Niedermann,George Caputa,Beth Kelly,Ursula Warthorst,Anne Rensing-Ehl,Ryan Kyle,Lana Vandersarren,Jonathan D. Curtis,Annette E. Patterson,Simon J. Lawless,Katarzyna M. Grzes,Jing Qiu,David E. Sanin,Oliver Kretz,Oliver Kretz,Tobias B. Huber,Tobias B. Huber,Sophie Janssens,Bart N. Lambrecht,Angelika S. Rambold,Edward J. Pearce,Erika L. Pearce +29 more
TL;DR: Early CD28-dependent mitochondrial engagement is needed for T cells to remodel cristae, develop SRC, and rapidly produce cytokines upon restimulation-cardinal features of protective memory T-cells.
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