| Preferential depletion of gut CD4-expressing iNKT cells contributes to systemic immune activation in HIV-1 infection. | |
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MedLine Citation:
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PMID: 23149661 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Chronic inappropriate immune activation is the central defect-driving loss of CD4(+) T helper cells and progression to AIDS in persons with HIV-1 infection, but the mechanisms remain controversial. We examined key regulatory invariant receptor natural killer T (iNKT) cells in the gut, the largest reservoir of lymphocytes and a key arena of HIV-1 pathogenesis. In healthy control persons, the anti-inflammatory CD4(+) iNKT-cell subset predominated over the pro-inflammatory CD4(-) iNKT-cell subset in the gut, but not in the blood, compartment. HIV-1 infection resulted in a preferential loss of this anti-inflammatory CD4(+) iNKT-cell subset within the gut. The degree of loss of the CD4(+) iNKT-cell subset in the gut, but not in the blood, correlated to the systemic immune activation and exhaustion that have been linked to disease progression. These results suggest a potentially important contribution of gut iNKT-cell imbalance in determining the systemic immune activation that is the hallmark of HIV-1 pathogenesis.Mucosal Immunology advance online publication 14 November 2012; doi:10.1038/mi.2012.101. |
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Authors:
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F J Ibarrondo; S B Wilson; L E Hultin; R Shih; M A Hausner; P M Hultin; P A Anton; B D Jamieson; O O Yang |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-11-14 |
Journal Detail:
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Title: Mucosal immunology Volume: - ISSN: 1935-3456 ISO Abbreviation: Mucosal Immunol Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-11-14 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101299742 Medline TA: Mucosal Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Department of Medicine and UCLA AIDS Institute, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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