Linked Life Data

17678476

Source:http://linkedlifedata.com/resource/pubmed/id/17678476

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2007-8-6
pubmed:abstractText
CD1d-restricted natural killer T (iNKT) cells are increasingly recognized as key immunoregulatory cells linking innate and adaptive immunity. These fall into functionally distinct CD4+ versus CD4- subsets that are believed to steer cellular immunity toward tolerigenic/atopic versus proinflammatory phenotypes, respectively. Preferential depletion of the CD4+ subset has been observed in HIV-1 infection, but the repletion of these cells after antiretroviral therapy has not been examined in detail. T lymphocytes, CD8+ lymphocyte activation, viremia, and iNKT cell subsets in peripheral blood were compared between 18 HIV-1-uninfected (Control) and 18 seropositive (SP) men initially not on suppressive antiretroviral therapy. Compared to the Control group, the SP group demonstrated reduction of CD4+ and lesser reduction of CD4- iNKT cells at baseline. After initiation of suppressive antiretroviral treatment, the SP CD4+ iNKT cell levels remained unchanged after a year and increased by 2 years, while CD4+ iNKT cells showed a gradual increase notable after the first year. Over the first year of treatment, there was a significant correlation between changes in total CD4+ T lymphocyte and changes in CD4+ iNKT cell levels, and a significant inverse correlation between changes in CD8+ T lymphocyte activation and changes in CD4- iNKT cell levels. These results confirm preferential depletion of tolerigenic/atopic CD4+ iNKT cells by HIV-1, and suggest that disproportionate persistence of proinflammatory CD4- iNKT cells could contribute to the inappropriate immune activation believed to cause immunodeficiency in HIV-1 infection.
pubmed:grant
http://linkedlifedata.com/resource/pubmed/grant/5-M01-RR-00722, http://linkedlifedata.com/resource/pubmed/grant/AI028697, http://linkedlifedata.com/resource/pubmed/grant/AI035040, http://linkedlifedata.com/resource/pubmed/grant/AI045051, http://linkedlifedata.com/resource/pubmed/grant/AI046130, http://linkedlifedata.com/resource/pubmed/grant/AI058845, http://linkedlifedata.com/resource/pubmed/grant/AI063974, http://linkedlifedata.com/resource/pubmed/grant/CA016042, http://linkedlifedata.com/resource/pubmed/grant/U01-AI-35039, http://linkedlifedata.com/resource/pubmed/grant/U01-AI-35040, http://linkedlifedata.com/resource/pubmed/grant/U01-AI-35041, http://linkedlifedata.com/resource/pubmed/grant/U01-AI-35042, http://linkedlifedata.com/resource/pubmed/grant/U01-AI-35043, http://linkedlifedata.com/resource/pubmed/grant/U01-AI-37613, http://linkedlifedata.com/resource/pubmed/grant/U01-AI-37984
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0889-2229
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
913-22
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Delayed reconstitution of CD4+ iNKT cells after effective HIV type 1 therapy.
pubmed:affiliation
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA. oyang@mednet.ucla.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural