Cosgrove, Cormac; Ussher, James E; Rauch, Andri; Gärtner, Kathleen; Kurioka, Ayako; Hühn, Michael H; Adelmann, Krista; Kang, Yu-Hoi; Fergusson, Joannah R; Simmonds, Peter; Goulder, Philip; Hansen, Ted H; Fox, Julie; Günthard, Huldrych F; Khanna, Nina; Powrie, Fiona; Steel, Alan; Gazzard, Brian; Phillips, Rodney E; Frater, John; ... (2012). Early and nonreversible decrease of CD161++ /MAIT cells in HIV infection. Blood, 121(6), pp. 951-61. Washington, D.C.: American Society of Hematology 10.1182/blood-2012-06-436436
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HIV infection is associated with immune dysfunction, perturbation of immune-cell subsets and opportunistic infections. CD161++ CD8+ T cells are a tissue-infiltrating population that produce IL17A, IL22, IFN, and TNFα, cytokines important in mucosal immunity. In adults they dominantly express the semi-invariant TCR Vα7.2, the canonical feature of mucosal associated invariant T (MAIT) cells and have been recently implicated in host defense against pathogens. We analyzed the frequency and function of CD161++ /MAIT cells in peripheral blood and tissue from patients with early stage or chronic-stage HIV infection. We show that the CD161++ /MAIT cell population is significantly decreased in early HIV infection and fails to recover despite otherwise successful treatment. We provide evidence that CD161++ /MAIT cells are not preferentially infected but may be depleted through diverse mechanisms including accumulation in tissues and activation-induced cell death. This loss may impact mucosal defense and could be important in susceptibility to specific opportunistic infections in HIV.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Infectiology |
UniBE Contributor: |
Rauch, Andri |
ISSN: |
0006-4971 |
Publisher: |
American Society of Hematology |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:37 |
Last Modified: |
05 Dec 2022 14:11 |
Publisher DOI: |
10.1182/blood-2012-06-436436 |
PubMed ID: |
23255555 |
Web of Science ID: |
000314868800016 |
BORIS DOI: |
10.7892/boris.14853 |
URI: |
https://boris.unibe.ch/id/eprint/14853 (FactScience: 221989) |