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Folly Beach Library
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Edgar Allan Poe/Sullivan's Island Library
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Wando Mount Pleasant Library
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Phone: (843) 805-6888
Village Library
9 a.m. – 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. – 8 p.m.
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Otranto Road Library
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McClellanville Library
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Keith Summey North Charleston Library
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Hurd/St. Andrews Library
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Phone: (843) 795-6679
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9 a.m. – 8 p.m.
Phone: (843) 805-6930
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The Role of KLRG1 in Human CD4+ T-Cell Immunity Against Tuberculosis.
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- Author(s): Zhidong Hu; Hui-Min Zhao; Chun-Ling Li; Xu-Hui Liu; Barkan, Daniel; Lowrie, Douglas B.; Shui-Hua Lu; Xiao-Yong Fan; Hu, Zhidong (AUTHOR); Zhao, Hui-Min (AUTHOR); Li, Chun-Ling (AUTHOR); Liu, Xu-Hui (AUTHOR); Lu, Shui-Hua (AUTHOR); Fan, Xiao-Yong (AUTHOR)
- Source:
Journal of Infectious Diseases. 5/1/2018, Vol. 217 Issue 9, p1491-1503. 13p. - Source:
- Additional Information
- Subject Terms:
- Abstract:
Background: KLRG1 is a marker of terminally differentiated CD8+ T cells in viral infection, but its role in human Mycobacterium tuberculosis infection remains elusive.Methods: A set of cohorts of patients with tuberculosis was designed, and the expression profiles and functions of KLRG1+CD4+ T cells were determined with and without antibody blocking.Results: KLRG1 expression on CD4+ T cells was significantly increased in patients with active tuberculosis, compared with healthy controls and patients without tuberculosis. Upon M. tuberculosis-specific stimulation, the ability to secrete interferon γ, interleukin 2, and tumor necrosis factor α was significantly greater in KLRG1-expressing CD4+ T cells than in their KLRG-negative counterparts and was accompanied by a decreased proportion of regulatory T cells and increased Akt signaling. However, KLRG1-expressing CD4+ T cells had a shorter life-span, which was associated with a higher apoptosis rate but a similar proliferative response. Blockade of KLRG1 signaling significantly enhanced interferon γ and interleukin 2 secretion without affecting either cell apoptosis or multiplication. Addition of a specific Akt inhibitor prevented this increased cytokine response, implicating the Akt signaling pathway.Conclusions: Our study delineated the profile of KLRG1+CD4+ T cells in patients with tuberculosis and suggests that M. tuberculosis infection drives CD4+ T cells to acquire increased effector function in a terminally differentiated state, which is restrained by KLRG1 via KLRG1/Akt signaling pathway. [ABSTRACT FROM AUTHOR] - Abstract: Copyright of Journal of Infectious Diseases is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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