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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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Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β.

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).
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Intrathymic programming of effector fates in three molecularly distinct γδ T cell subtypes

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.
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Tuberculosis Susceptibility of Diabetic Mice

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.
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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.