Michael T. Waring
Ragon Institute of MGH, MIT and Harvard
30 Papers
131 Citations
Michael T. Waring is an academic researcher from Ragon Institute of MGH, MIT and Harvard. The author has contributed to research in topics: Cytotoxic T cell & CD8. The author has an hindex of 19, co-authored 29 publications. Previous affiliations of Michael T. Waring include Massachusetts Institute of Technology & Harvard University.
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Papers
Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4a.
Viktor Janzen,Randolf Forkert,Heather E. Fleming,Yoriko Saito,Michael T. Waring,David Dombkowski,Tao Cheng,Tao Cheng,Ronald A. DePinho,Norman E. Sharpless,David T. Scadden +10 more
TL;DR: It is reported that the cyclin-dependent kinase inhibitor p16INK4a accumulates and modulates specific age-associated HSC functions, and may ameliorate the physiological impact of ageing on stem cells and thereby improve injury repair in aged tissue.
1.1K
Myocardial infarction accelerates atherosclerosis
Partha Dutta,Gabriel Courties,Ying Wei,Florian Leuschner,Florian Leuschner,Rostic Gorbatov,Clinton S. Robbins,Yoshiko Iwamoto,Brian Thompson,Alicia L. Carlson,Timo Heidt,Maulik D. Majmudar,Maulik D. Majmudar,Felix Lasitschka,Martin Etzrodt,Peter Waterman,Michael T. Waring,Michael T. Waring,Adam T. Chicoine,Adam T. Chicoine,Anja M. van der Laan,Hans W.M. Niessen,Jan J. Piek,Barry B. Rubin,Jagdish Butany,James R. Stone,Hugo A. Katus,Sabina A. Murphy,David A. Morrow,Marc S. Sabatine,Claudio Vinegoni,Michael A. Moskowitz,Mikael J. Pittet,Peter Libby,Charles P. Lin,Filip K. Swirski,Ralph Weissleder,Matthias Nahrendorf +37 more
TL;DR: It is shown that the systemic response to ischaemic injury aggravates chronic atherosclerosis and provides a novel therapeutic opportunity to mitigate disease progression.
Loss of Bcl-6-Expressing T Follicular Helper Cells and Germinal Centers in COVID-19.
Naoki Kaneko,Hsiao-Hsuan Kuo,Julie Boucau,Jocelyn R. Farmer,Hugues Allard-Chamard,Vinay Mahajan,Alicja Piechocka-Trocha,Kristina Lefteri,Matthew Osborn,Julia Bals,Yannic C. Bartsch,Nathalie Bonheur,Timothy M. Caradonna,Josh Chevalier,Fatema Z. Chowdhury,Thomas J. Diefenbach,Kevin Einkauf,Jon Fallon,Jared Feldman,Kelsey K. Finn,Pilar Garcia-Broncano,Ciputra Adijaya Hartana,Blake M. Hauser,Chenyang Jiang,Paulina Kaplonek,Marshall Karpell,Eric C. Koscher,Xiao-Dong Lian,Hang Liu,Jinqing Liu,Ngoc L. Ly,Ashlin R. Michell,Yelizaveta Rassadkina,Kyra Seiger,Libera Sessa,Sally Shin,Nishant K. Singh,Weiwei Sun,Xiaoming Sun,Hannah J. Ticheli,Michael T. Waring,Alex Lee Zhu,Galit Alter,Jonathan Z. Li,Daniel Lingwood,Aaron G. Schmidt,Mathias Lichterfeld,Bruce D. Walker,Xu G. Yu,Robert F. Padera,Shiv Pillai +50 more
TL;DR: Data identify defective Bcl-6+ TFH cell generation and dysregulated humoral immune induction early in COVID-19 disease, providing a mechanistic explanation for the limited durability of antibody responses in coronavirus infections and suggest that achieving herd immunity through natural infection may be difficult.
729
Upregulation of CTLA-4 by HIV-specific CD4+ T cells correlates with disease progression and defines a reversible immune dysfunction.
Daniel Kaufmann,Daniel G. Kavanagh,Florencia Pereyra,Florencia Pereyra,John Zaunders,Elizabeth W Mackey,Toshiyuki Miura,Toshiyuki Miura,Sarah Palmer,Mark A. Brockman,Mark A. Brockman,Almas Rathod,Alicja Piechocka-Trocha,Alicja Piechocka-Trocha,Brett Baker,Baogong Zhu,Sylvie Le Gall,Michael T. Waring,Michael T. Waring,Ryan Ahern,Kristin Moss,Anthony D. Kelleher,John M. Coffin,Gordon J. Freeman,Eric S. Rosenberg,Bruce D. Walker,Bruce D. Walker +26 more
TL;DR: It is reported that the inhibitory immunoregulatory receptor CTLA-4 was selectively upregulated in human immunodeficiency virus–specific CD4+ T cells but not CD8- T cells in all categories of HIV-infected subjects evaluated, with the exception of rare people able to control viremia in the absence of antiretroviral therapy.
568
Innate Response Activator B Cells Protect Against Microbial Sepsis
Philipp J. Rauch,Aleksey Chudnovskiy,Clinton S. Robbins,Georg F. Weber,Martin Etzrodt,Ingo Hilgendorf,Elizabeth Tiglao,Jose-Luiz Figueiredo,Yoshiko Iwamoto,Igor Theurl,Rostic Gorbatov,Michael T. Waring,Adam Chicoine,Majd Mouded,Mikael J. Pittet,Matthias Nahrendorf,Ralph Weissleder,Filip K. Swirski +17 more
TL;DR: An effector B cell population that protects against microbial sepsis is described that is phenotypically and functionally distinct, develop and diverge from B1a B cells, depend on pattern-recognition receptors, and produce granulocyte-macrophage colony-stimulating factor.