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Patricia A. Sheridan

Researcher at University of North Carolina at Chapel Hill

Publications -  26
Citations -  2124

Patricia A. Sheridan is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Immune system & CD8. The author has an hindex of 17, co-authored 26 publications receiving 1831 citations. Previous affiliations of Patricia A. Sheridan include University of Rochester.

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Obesity is associated with impaired immune response to influenza vaccination in humans

TL;DR: Results suggest obesity may impair the ability to mount a protective immune response to influenza virus, and PBMCs challenged ex vivo with vaccine strain virus demonstrated that obese individuals had decreased CD8+ T-cell activation and decreased expression of functional proteins compared with healthy weight individuals.
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Diet-Induced Obese Mice Have Increased Mortality and Altered Immune Responses When Infected with Influenza Virus

TL;DR: The data indicate that obesity inhibits the ability of the immune system to appropriately respond to influenza infection and suggests that obesity may lead to increased morbidity and mortality from viral infections.
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Diet-induced obesity impairs the T cell memory response to influenza virus infection.

TL;DR: In this article, a secondary H1N1 influenza challenge following a primary H3N2 infection led to a 25% mortality rate (with no loss of lean controls), 25% increase in lung pathology, failure to regain weight, and 10- to 100-fold higher lung viral titers.
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Overweight and obese adult humans have a defective cellular immune response to pandemic H1N1 Influenza a virus

TL;DR: The objective of the present study was to elucidate the specific mechanisms by which obesity and overweight impact the cellular immune response to pH1N1.
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Selective impairment in dendritic cell function and altered antigen-specific CD8+ T-cell responses in diet-induced obese mice infected with influenza virus.

TL;DR: Obese mice displayed aberrant innate immune responses characterized by minimal induction of interferon, delayed expression of pro‐inflammatory cytokines and chemokines, and impaired natural killer cell cytotoxicity, leading to alterations in the T‐cell population that ultimately may be detrimental to the host.