G
Gregory W. Martens
Researcher at University of Massachusetts Medical School
Publications - 21
Citations - 1897
Gregory W. Martens is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Cytotoxic T cell & T cell. The author has an hindex of 18, co-authored 21 publications receiving 1701 citations. Previous affiliations of Gregory W. Martens include Baylor University Medical Center & University of California, Davis.
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Journal ArticleDOI
Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β.
Bibhuti B. Mishra,Vijay A. K. Rathinam,Gregory W. Martens,Amanda J. Martinot,Hardy Kornfeld,Katherine A. Fitzgerald,Christopher M. Sassetti,Christopher M. Sassetti +7 more
TL;DR: By exogenously controlling the replication of Mycobacterium tuberculosis in vivo, the requirement for antimicrobial immunity is obviated and it is discovered that both IL-1 production and infection-induced immunopathology were suppressed by lymphocyte-derived interferon-γ (IFN-γ).
Journal ArticleDOI
Intrathymic programming of effector fates in three molecularly distinct γδ T cell subtypes
Kavitha Narayan,Katelyn Sylvia,Nidhi Malhotra,Catherine C. Yin,Gregory W. Martens,Therese Vallerskog,Hardy Kornfeld,Na Xiong,Nadia Cohen,Michael B. Brenner,Leslie J. Berg,Joonsoo Kang +11 more
TL;DR: A high-resolution transcriptome analysis of all emergent γδ thymocyte subsets segregated on the basis of use of the TCR γ-chain or δ-chain indicated the existence of three separate subtypes of γ δ effector cells in the thymus, each distinguished by unique transcription-factor modules that program effector function.
Journal ArticleDOI
Tuberculosis Susceptibility of Diabetic Mice
Gregory W. Martens,Meltem Cevik Arikan,Jinhee Lee,Fucheng Ren,Dale L. Greiner,Hardy Kornfeld +5 more
TL;DR: It is shown that Mtb infection of STZ-treated mice provides a useful model to study the effects of hyperglycemia on immunity, and indicates that the initiation of adaptive immunity is impaired by chronic hyper glycemia, resulting in a higher steady-state burden of Mtb in the lung.
Intrathymic programming of effector fates in three molecularly distinct γδ T cell subtypes
Kavitha Narayan,Katelyn E Sylvia,Nidhi Malhotra,Catherine C. Yin,Gregory W. Martens,Therese Vallerskog,Hardy Kornfeld,Na Xiong,Nadia R Cohen,Michael B. Brenner,Leslie J. Berg,Joonsoo Kang,Yan Zhou,Susan A. Shinton,Richard R. Hardy,Natalie A. Bezman,Joseph C. Sun,Charles C. Kim,Lewis L. Lanier,Jennifer Miller,Brian D. Brown,Miriam Merad,Anne L. Fletcher,Kutlu G. Elpek,Angelique Bellemare-Pelletier,Deepali Malhotra,Shannon J. Turley,Katelyn Sylvia,Roi Gazit,Brian S. Garrison,Derrick J. Rossi,Vladimir Jojic,Daphne Koller,Radu Jianu,David H. Laidlaw,James C. Costello,James J. Collins,Nadia Cohen,Patrick J. Brennan,Michael Brenner,Tal Shay,Aviv Regev,Francis Kim,Tata Nageswara Rao,Amy J. Wagers,Emmanuel L. Gautier,Claudia Jakubzick,Gwendalyn J. Randolph,Paul A. Monach,Adam J Best,Jamie Knell,Ananda W. Goldrath,Tracy Heng,Taras Kreslavsky,Michio W. Painter,Diane Mathis,Christophe Benoist +56 more
Journal ArticleDOI
Diabetic Mice Display a Delayed Adaptive Immune Response to Mycobacterium tuberculosis
TL;DR: It is concluded that TB increased susceptibility in DM results from a delayed innate immune response to the presence of M. tuberculosis-infected alveolar macrophages, which causes late delivery of Ag-bearing APC to the lung draining LNs and delayed priming of the adaptive immune response that is necessary to restrict M. TB replication.