NDLI: CD14++CD16+ Monocytes Are Enriched by Glucocorticoid Treatment and Are Functionally Attenuated in Driving Effector T Cell Responses.

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CD14++CD16+ Monocytes Are Enriched by Glucocorticoid Treatment and Are Functionally Attenuated in Driving Effector T Cell Responses.

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CD14++CD16+ Monocytes Are Enriched by Glucocorticoid Treatment and Are Functionally Attenuated in Driving Effector T Cell Responses.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wei, Lai Chien, Jason L. Si, Han Dhanda, Ashwin Casady, Megan Jawad, Shayma Williams, Emily L. Lee, Richard W. J. Nussenblatt, Robert B. Sen, H. Nida Dailey, Jennifer Ling, Diamond Chen, Ping Liu, Baoying Martinez Estrada, Fernando Tucker, William Li, Zhiyu Gordon, Siamon Thompson, Ian Hannes, Susan Hirani, Sima Sura, Amol
Description	Author Affiliation: Liu B ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Dhanda A ( School of Clinical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom); Hirani S ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Williams EL ( School of Clinical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom); Sen HN ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Martinez Estrada F ( Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom.); Ling D ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Thompson I ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Casady M ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Li Z ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Si H ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Tucker W ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Wei L ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Jawad S ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Sura A ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Dailey J ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Hannes S ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Chen P ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Chien JL ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892); Gordon S ( Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom.); Lee RW ( School of Clinical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom); Nussenblatt RB ( Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892)
Abstract	Human peripheral monocytes have been categorized into three subsets based on differential expression levels of CD14 and CD16. However, the factors that influence the distribution of monocyte subsets and the roles that each subset plays in autoimmunity are not well studied. In this study, we show that circulating monocytes from patients with autoimmune uveitis exhibit a skewed phenotype toward intermediate CD14(++)CD16(+) cells, and that this is associated with glucocorticoid therapy. We further demonstrate that CD14(++)CD16(+) monocytes from patients and healthy control donors share a similar cell-surface marker and gene expression profile. Comparison of the effects of intermediate CD14(++)CD16(+) monocytes with classical CD14(++)CD16(-) and nonclassical CD14(+)CD16(++) monocytes revealed that the intermediate CD14(++)CD16(+) subset had an attenuated capacity to promote both naive CD4(+) T cell proliferation and polarization into a Th1 phenotype, and memory CD4(+) T cell proliferation and IL-17 expression. Furthermore, CD14(++)CD16(+) cells inhibit CD4(+) T cell proliferation induced by other monocyte subsets and enhance CD4(+) T regulatory cell IL-10 expression. These data demonstrate the impact of glucocorticoids on monocyte phenotype in the context of autoimmune disease and the differential effects of monocyte subsets on effector T cell responses.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1402409
Journal	The Journal of Immunology
Issue Number	11
Volume Number	194
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd14 Metabolism Glucocorticoids Pharmacology Leukocytes, Mononuclear Immunology Receptors, Igg T-lymphocytes, Regulatory Autoimmune Diseases Autoimmunity Cell Differentiation Cell Proliferation Cells, Cultured Dexamethasone Gpi-linked Proteins Interferon-gamma Biosynthesis Interleukin-10 Interleukin-17 Lymphocyte Activation Th1 Cells Cytology Uveitis 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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