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Manoj Thapa

Researcher at Emory University

Publications -  21
Citations -  775

Manoj Thapa is an academic researcher from Emory University. The author has contributed to research in topics: Chemokine & Immune system. The author has an hindex of 12, co-authored 21 publications receiving 629 citations. Previous affiliations of Manoj Thapa include University of Oklahoma Health Sciences Center & Yerkes National Primate Research Center.

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Hepatic Stellate Cells Preferentially Induce Foxp3+ Regulatory T Cells by Production of Retinoic Acid

TL;DR: It is concluded that HSCs preferentially generate Foxp3+ Tregs and, therefore, may play a role in the tolerogenic nature of the liver.
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Susceptibility of CCR5-Deficient Mice to Genital Herpes Simplex Virus Type 2 Is Linked to NK Cell Mobilization

TL;DR: The absence of CCR5 expression significantly impacts the ability of the host to control genital HSV-2 infection, inflammation, and spread associated with a specific reduction in NK cell expansion, infiltration, and activity in the nervous system.
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CXCL9 and CXCL10 Expression Are Critical for Control of Genital Herpes Simplex Virus Type 2 Infection through Mobilization of HSV-Specific CTL and NK Cells to the Nervous System

TL;DR: The absence of CXCL9 or CxCL10 expression significantly alters the ability of the host to control genital HSV-2 infection through the mobilization of effector cells to sites of infection.
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Alterations in Intestinal Microbiota Lead to Production of Interleukin 17 by Intrahepatic γδ T-Cell Receptor–Positive Cells and Pathogenesis of Cholestatic Liver Disease

TL;DR: Development of liver fibrosis and inflammation to require hepatic activation of γδ TCR+ cells and production of IL17 mediated by exposure to L gasseri appears to contribute to development of cholestatic liver disease in patients.
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Intact TRL 9 and type I interferon signaling pathways are required to augment HSV-1 induced corneal CXCL9 and CXCL10.

TL;DR: This is the first report that shows enhanced CXCL10 expression following neurotropic viral replication requires both intact TLR 9 and type I interferon signaling pathways, and is correlative with an increase in virus shedding and a reduction in neutrophil infiltration.