NDLI: Tim-3 pathway controls regulatory and effector T cell balance during hepatitis C virus infection.

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Tim-3 pathway controls regulatory and effector T cell balance during hepatitis C virus infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Jia M. Ma, Cheng J. Wang, Ke S. Moorman, Jonathan P. Yao, Zhi Q. Zhang, Ying Wu, Xiao Y. Ji, Xiao J. Jia, Zhan S.
Description	Country affiliation: United States Author Affiliation: Moorman JP ( Department of Veterans Affairs, James H. Quillen Veterans Affairs Medical Center, Johnson City, TN 37614, USA.)
Abstract	Hepatitis C virus (HCV) is remarkable at disrupting human immunity to establish chronic infection. Upregulation of inhibitory signaling pathways (such as T cell Ig and mucin domain protein-3 [Tim-3]) and accumulation of regulatory T cells (Tregs) play pivotal roles in suppressing antiviral effector T cell (Teff) responses that are essential for viral clearance. Although the Tim-3 pathway has been shown to negatively regulate Teffs, its role in regulating Foxp3(+) Tregs is poorly explored. In this study, we investigated whether and how the Tim-3 pathway alters Foxp3(+) Treg development and function in patients with chronic HCV infection. We found that Tim-3 was upregulated, not only on IL-2-producing CD4(+)CD25(+)Foxp3(-) Teffs, but also on CD4(+)CD25(+)Foxp3(+) Tregs, which accumulate in the peripheral blood of chronically HCV-infected individuals when compared with healthy subjects. Tim-3 expression on Foxp3(+) Tregs positively correlated with expression of the proliferation marker Ki67 on Tregs, but it was inversely associated with proliferation of IL-2-producing Teffs. Moreover, Foxp3(+) Tregs were found to be more resistant to, and Foxp3(-) Teffs more sensitive to, TCR activation-induced cell apoptosis, which was reversible by blocking Tim-3 signaling. Consistent with its role in T cell proliferation and apoptosis, blockade of Tim-3 on CD4(+)CD25(+) T cells promoted expansion of Teffs more substantially than Tregs through improving STAT-5 signaling, thus correcting the imbalance of Foxp3(+) Tregs/Foxp3(-) Teffs that was induced by HCV infection. Taken together, the Tim-3 pathway appears to control Treg and Teff balance through altering cell proliferation and apoptosis during HCV infection.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200162
Journal	The Journal of Immunology
Issue Number	2
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Hepatitis C, Chronic Immunology Pathology Receptors, Immunologic Physiology Signal Transduction T-lymphocyte Subsets Virology T-lymphocytes, Regulatory Apoptosis Regulatory Proteins Cell Proliferation Forkhead Transcription Factors Biosynthesis Metabolism Interleukin-2 Receptor Alpha Subunit Pilot Projects Viremia Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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