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Alexander Pichugin

Researcher at Walter Reed Army Institute of Research

Publications -  26
Citations -  662

Alexander Pichugin is an academic researcher from Walter Reed Army Institute of Research. The author has contributed to research in topics: Antigen & Immune system. The author has an hindex of 13, co-authored 26 publications receiving 577 citations. Previous affiliations of Alexander Pichugin include Harvard University & Russian Academy.

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Dominant role of the sst1 locus in pathogenesis of necrotizing lung granulomas during chronic tuberculosis infection and reactivation in genetically resistant hosts.

TL;DR: It is demonstrated that within the complex, multigenic architecture of tuberculosis susceptibility, sst1 functions to control necrosis within tuberculosis lesions in the lungs; this lung-specific sst 1 effect is independent of both the route of infection and genetic background of the host.
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Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control.

TL;DR: Experimental evidence that chronic TB infection induces cell dysplasia and squamous cell carcinoma in a lung-specific manner is presented and a genetic model for further analysis of carcinogenic mechanisms activated by TB infection is established.
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Comparative Analysis of T Lymphocytes Recovered from the Lungs of Mice Genetically Susceptible, Resistant, and Hyperresistant to Mycobacterium tuberculosis-Triggered Disease

TL;DR: Parameters of lung T cell activation and response following M. tuberculosis challenge are compared to find a more balanced type of immune reactivity that could be linked to a better TB defense.
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Progression of Pulmonary Tuberculosis and Efficiency of Bacillus Calmette-Guérin Vaccination Are Genetically Controlled via a Common sst1-Mediated Mechanism of Innate Immunity

TL;DR: The data suggest that in immunocompetent humans the development of pulmonary tuberculosis and the failure of the existing vaccine to protect against it, in some cases, may be explained by a similar defect in a conserved inducible NO synthase-independent mechanism of innate immunity, either inherited or acquired.