Emerging role and characterization of immunometabolism

Relevance to HIV pathogenesis, serious non-AIDS events, and a cure

Clovis S. Palmer, Darren C. Henstridge, Di Yu, Amit Singh, Brad Balderson, Gabriel Duette, Catherine L. Cherry, Joshua J. Anzinger, Matias Ostrowski, Suzanne M. Crowe

Research output: Contribution to journalReview ArticleOtherpeer-review

12 Citations (Scopus)

Abstract

Immune cells cycle between a resting and an activated state. Their metabolism is tightly linked to their activation status and, consequently, functions. Ag recognition induces T lymphocyte activation and proliferation and acquisition of effector functions that require and depend on cellular metabolic reprogramming. Likewise, recognition of pathogen-associated molecular patterns by monocytes and macrophages induces changes in cellular metabolism. As obligate intracellular parasites, viruses manipulate the metabolism of infected cells to meet their structural and functional requirements. For example, HIV-induced changes in immune cell metabolism and redox state are associated with CD4+ T cell depletion, immune activation, and inflammation. In this review, we highlight how HIV modifies immunometabolism with potential implications for cure research and pathogenesis of comorbidities observed in HIV-infected patients, including those with virologic suppression. In addition, we highlight recently described key methods that can be applied to study the metabolic dysregulation of immune cells in disease states.
Original languageEnglish
Pages (from-to)4437-4444
Number of pages8
JournalJournal of Immunology
Volume196
Issue number11
DOIs
Publication statusPublished - 1 Jun 2016

Cite this

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title = "Emerging role and characterization of immunometabolism: Relevance to HIV pathogenesis, serious non-AIDS events, and a cure",
abstract = "Immune cells cycle between a resting and an activated state. Their metabolism is tightly linked to their activation status and, consequently, functions. Ag recognition induces T lymphocyte activation and proliferation and acquisition of effector functions that require and depend on cellular metabolic reprogramming. Likewise, recognition of pathogen-associated molecular patterns by monocytes and macrophages induces changes in cellular metabolism. As obligate intracellular parasites, viruses manipulate the metabolism of infected cells to meet their structural and functional requirements. For example, HIV-induced changes in immune cell metabolism and redox state are associated with CD4+ T cell depletion, immune activation, and inflammation. In this review, we highlight how HIV modifies immunometabolism with potential implications for cure research and pathogenesis of comorbidities observed in HIV-infected patients, including those with virologic suppression. In addition, we highlight recently described key methods that can be applied to study the metabolic dysregulation of immune cells in disease states.",
author = "Palmer, {Clovis S.} and Henstridge, {Darren C.} and Di Yu and Amit Singh and Brad Balderson and Gabriel Duette and Cherry, {Catherine L.} and Anzinger, {Joshua J.} and Matias Ostrowski and Crowe, {Suzanne M.}",
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Emerging role and characterization of immunometabolism : Relevance to HIV pathogenesis, serious non-AIDS events, and a cure. / Palmer, Clovis S.; Henstridge, Darren C.; Yu, Di; Singh, Amit; Balderson, Brad; Duette, Gabriel; Cherry, Catherine L.; Anzinger, Joshua J.; Ostrowski, Matias; Crowe, Suzanne M.

In: Journal of Immunology, Vol. 196, No. 11, 01.06.2016, p. 4437-4444.

Research output: Contribution to journalReview ArticleOtherpeer-review

TY - JOUR

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AU - Henstridge, Darren C.

AU - Yu, Di

AU - Singh, Amit

AU - Balderson, Brad

AU - Duette, Gabriel

AU - Cherry, Catherine L.

AU - Anzinger, Joshua J.

AU - Ostrowski, Matias

AU - Crowe, Suzanne M.

PY - 2016/6/1

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N2 - Immune cells cycle between a resting and an activated state. Their metabolism is tightly linked to their activation status and, consequently, functions. Ag recognition induces T lymphocyte activation and proliferation and acquisition of effector functions that require and depend on cellular metabolic reprogramming. Likewise, recognition of pathogen-associated molecular patterns by monocytes and macrophages induces changes in cellular metabolism. As obligate intracellular parasites, viruses manipulate the metabolism of infected cells to meet their structural and functional requirements. For example, HIV-induced changes in immune cell metabolism and redox state are associated with CD4+ T cell depletion, immune activation, and inflammation. In this review, we highlight how HIV modifies immunometabolism with potential implications for cure research and pathogenesis of comorbidities observed in HIV-infected patients, including those with virologic suppression. In addition, we highlight recently described key methods that can be applied to study the metabolic dysregulation of immune cells in disease states.

AB - Immune cells cycle between a resting and an activated state. Their metabolism is tightly linked to their activation status and, consequently, functions. Ag recognition induces T lymphocyte activation and proliferation and acquisition of effector functions that require and depend on cellular metabolic reprogramming. Likewise, recognition of pathogen-associated molecular patterns by monocytes and macrophages induces changes in cellular metabolism. As obligate intracellular parasites, viruses manipulate the metabolism of infected cells to meet their structural and functional requirements. For example, HIV-induced changes in immune cell metabolism and redox state are associated with CD4+ T cell depletion, immune activation, and inflammation. In this review, we highlight how HIV modifies immunometabolism with potential implications for cure research and pathogenesis of comorbidities observed in HIV-infected patients, including those with virologic suppression. In addition, we highlight recently described key methods that can be applied to study the metabolic dysregulation of immune cells in disease states.

UR - http://www.ncbi.nlm.nih.gov/pubmed/27207806

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