title: Chronic exposure to type-I IFN under lymphopenic conditions alters CD4 T cell homeostasis.
abstract: HIV infection and the associated chronic immune activation alter T cell homeostasis leading to CD4 T cell depletion and CD8 T cell expansion. The mechanisms behind these outcomes are not totally defined and only partially explained by the direct cytopathic effect of the virus. In this manuscript, we addressed the impact of lymphopenia and chronic exposure to IFN-α on T cell homeostasis. In a lymphopenic murine model, this interaction led to decreased CD4 counts and CD8 T cell expansion in association with an increase in the Signal Transducer and Activator of Transcription 1 (STAT1) levels resulting in enhanced CD4 T cell responsiveness to IFN-α. Thus, in the setting of HIV infection, chronic stimulation of this pathway could be detrimental for CD4 T cell homeostasis.
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Cecile
authors.initials: C
authors.lastname: Le Saout
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Rebecca B
authors.initials: RB
authors.lastname: Hasley
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Hiromi
authors.initials: H
authors.lastname: Imamichi
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Lueng
authors.initials: L
authors.lastname: Tcheung
authors.affiliation: Biostatistics Research Branch, DCR, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Zonghui
authors.initials: Z
authors.lastname: Hu
authors.affiliation: Experimental Immunology Branch, CCR, NCI, NIH, Bethesda, Maryland, United States of America.
authors.forename: Megan A
authors.initials: MA
authors.lastname: Luckey
authors.affiliation: Experimental Immunology Branch, CCR, NCI, NIH, Bethesda, Maryland, United States of America.
authors.forename: Jung-Hyun
authors.initials: JH
authors.lastname: Park
authors.affiliation: Laboratory of Immunoregulation, CCR, NCI, NIH, Frederick, Maryland, United States of America.
authors.forename: Scott K
authors.initials: SK
authors.lastname: Durum
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Mindy
authors.initials: M
authors.lastname: Smith
authors.affiliation: AIDS Monitoring Labs. Leidos Biomedical Research, Inc, Frederick, Maryland, United States of America.
authors.forename: Adam W
authors.initials: AW
authors.lastname: Rupert
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Michael C
authors.initials: MC
authors.lastname: Sneller
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: H Clifford
authors.initials: HC
authors.lastname: Lane
authors.affiliation: CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, Maryland, United States of America.
authors.forename: Marta
authors.initials: M
authors.lastname: Catalfamo
mesh_terms: D000818:Animals; D015153:Blotting, Western; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005434:Flow Cytometry; D015658:HIV Infections / Q000276:immunology*; D006706:Homeostasis / Q000276:immunology*; D006801:Humans; D007370:Interferon Type I / Q000276:immunology*; D008231:Lymphopenia / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout
chemical_list: D007370:Interferon Type I