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HIV-1 and SIV Infection Are Associated with Early Loss of Lung Interstitial CD4+ T Cells and Dissemination of Pulmonary Tuberculosis.
Corleis, Björn; Bucsan, Allison N; Deruaz, Maud; Vrbanac, Vladimir D; Lisanti-Park, Antonella C; Gates, Samantha J; Linder, Alice H; Paer, Jeffrey M; Olson, Gregory S; Bowman, Brittany A; Schiff, Abigail E; Medoff, Benjamin D; Tager, Andrew M; Luster, Andrew D; Khader, Shabaana A; Kaushal, Deepak; Kwon, Douglas S.
Affiliation
  • Corleis B; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: bcorleis@mgh.harvard.edu.
  • Bucsan AN; Tulane National Primate Research Center, Covington, LA, USA; Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, LA, USA.
  • Deruaz M; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
  • Vrbanac VD; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
  • Lisanti-Park AC; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Gates SJ; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Linder AH; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Paer JM; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Olson GS; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Bowman BA; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Schiff AE; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Medoff BD; Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA; Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA, USA.
  • Tager AM; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA; Division of Pulmonary and Critical Care Medicine, Massa
  • Luster AD; Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
  • Khader SA; Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO, USA.
  • Kaushal D; Tulane National Primate Research Center, Covington, LA, USA; Southwest National Primate Research Center, San Antonio, TX, USA.
  • Kwon DS; Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Division of Infectious Diseases, Massachusetts General Hospital, Boston, MA, USA.
Cell Rep ; 26(6): 1409-1418.e5, 2019 02 05.
Article de En | MEDLINE | ID: mdl-30726727
ABSTRACT
Lung interstitial CD4+ T cells are critical for protection against pulmonary infections, but the fate of this population during HIV-1 infection is not well described. We studied CD4+ T cells in the setting of HIV-1 infection in human lung tissue, humanized mice, and a Mycobacterium tuberculosis (Mtb)/simian immunodeficiency virus (SIV) nonhuman primate co-infection model. Infection with a CCR5-tropic strain of HIV-1 or SIV results in severe and rapid loss of lung interstitial CD4+ T cells but not blood or lung alveolar CD4+ T cells. This is accompanied by high HIV-1 production in these cells in vitro and in vivo. Importantly, during early SIV infection, loss of lung interstitial CD4+ T cells is associated with increased dissemination of pulmonary Mtb infection. We show that lung interstitial CD4+ T cells serve as an efficient target for HIV-1 and SIV infection that leads to their early depletion and an increased risk of disseminated tuberculosis.
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Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Tuberculose pulmonaire / Lymphocytes T CD4/ / Infections à VIH / Syndrome d'immunodéficience acquise du singe / Co-infection Type d'étude: Risk_factors_studies Limites: Animals / Female / Humans Langue: En Journal: Cell Rep Année: 2019 Type de document: Article
Texte intégral
Ajouter à My VHL
Imprimer
XML
PubMed Links
Recherche sur Google

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Tuberculose pulmonaire / Lymphocytes T CD4/ / Infections à VIH / Syndrome d'immunodéficience acquise du singe / Co-infection Type d'étude: Risk_factors_studies Limites: Animals / Female / Humans Langue: En Journal: Cell Rep Année: 2019 Type de document: Article