NDLI: Immune memory-boosting dose of rapamycin impairs macrophage vesicle acidification and curtails glycolysis in effector CD8 cells, impairing defense against acute infections.

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Immune memory-boosting dose of rapamycin impairs macrophage vesicle acidification and curtails glycolysis in effector CD8 cells, impairing defense against acute infections.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Goldberg, Emily L. Uhrlaub, Jennifer L. Lutes, Lydia K. Nikolich-Zugich, Janko Smithey, Megan J.
Description	Author Affiliation: Goldberg EL ( Department of Immunobiology, University of Arizona College of Medicine, Tucson, AZ 85724); Smithey MJ ( Department of Immunobiology, University of Arizona College of Medicine, Tucson, AZ 85724); Lutes LK ( Department of Immunobiology, University of Arizona College of Medicine, Tucson, AZ 85724); Uhrlaub JL ( Department of Immunobiology, University of Arizona College of Medicine, Tucson, AZ 85724); Nikolich-Zugich J ( Department of Immunobiology, University of Arizona College of Medicine, Tucson, AZ 85724)
Abstract	Direct mammalian target of rapamycin (Rapa) complex 1 inhibition by short-term low-dose Rapa treatment has recently been shown to improve CD8 T cell immunological memory. Whereas these studies focused on memory development, the impact of low-dose Rapa on the primary immune response, particularly as it relates to functional effector immunity, is far less clear. In this study, we investigated the impact of acute Rapa treatment on immune effector cell function during the primary immune response to several acute infections. We found that functional CD8 T cell and macrophage responses to both viral and intracellular bacterial pathogens were depressed in mice in vivo and in humans to phorbol ester and calcium ionophore stimulation in vitro in the face of low-dose Rapa treatment. Mechanistically, the CD8 defect was linked to impaired glycolytic switch in stimulated naive cells and the reduced formation of short-lived effector cells. Therefore, more than one cell type required for a protective effector immune response is impaired by Rapa in both mice and humans, at the dose shown to improve immune memory and extend lifespan. This urges caution with regard to the relative therapeutic costs and benefits of Rapa treatment as means to improve immune memory.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400188
Journal	The Journal of Immunology
Issue Number	2
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Drug Effects Macrophages Sirolimus Pharmacology T-lymphocyte Subsets Animals Immunology Metabolism Cells, Cultured Dose-response Relationship, Drug Flow Cytometry Glycolysis Granzymes Host-pathogen Interactions Hydrogen-ion Concentration Immunologic Memory Immunosuppressive Agents Interferon-gamma Listeria Monocytogenes Physiology Listeriosis Microbiology Prevention & Control Lymphocytic Choriomeningitis Virology Lymphocytic Choriomeningitis Virus Lysosomes Chemistry Mice Mice, Inbred C57bl Tumor Necrosis Factor-alpha Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Immune memory-boosting dose of rapamycin impairs macrophage vesicle acidification and curtails glycolysis in effector CD8 cells, impairing defense against acute infections

Protein energy malnutrition impairs homeostatic proliferation of memory CD8 T cells.

Sustained and incomplete recovery of naive CD8+ T cell precursors after sepsis contributes to impaired CD8+ T cell responses to infection.

B cell depletion curtails CD4+ T cell memory and reduces protection against disseminating virus infection.

Temporal requirements for B cells in the establishment of CD4 T cell memory.

PI3KÎ´ Regulates the Magnitude of CD8+ T Cell Responses after Challenge with Listeria monocytogenes.

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Lifelong persistent viral infection alters the naive T cell pool, impairing CD8 T cell immunity in late life.

Histone acetylation at the single-cell level: a marker of memory CD8+ T cell differentiation and functionality.

Immune memory-boosting dose of rapamycin impairs macrophage vesicle acidification and curtails glycolysis in effector CD8 cells, impairing defense against acute infections.

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Immune memory-boosting dose of rapamycin impairs macrophage vesicle acidification and curtails glycolysis in effector CD8 cells, impairing defense against acute infections.