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Titolo:
IFN-beta mediates coordinate expression of antigen-processing genes in RSV-infected pulmonary epithelial cells
Autore:
Jamaluddin, M; Wang, SF; Garofalo, RP; Elliott, T; Casola, A; Baron, S; Brasier, AR;
Indirizzi:
Univ Texas, Med Branch, Div Endocrinol, Dept Med, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 inol, Dept Med, Galveston, TX 77555 USA Univ Texas, Med Branch, Dept Pediat, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 h, Dept Pediat, Galveston, TX 77555 USA Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 biol & Immunol, Galveston, TX 77555 USA Univ Texas, Med Branch, Sealy Ctr Mol Sci, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 ly Ctr Mol Sci, Galveston, TX 77555 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 2, volume: 280, anno: 2001,
pagine: L248 - L257
SICI:
1040-0605(200102)280:2<L248:IMCEOA>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY SYNCYTIAL VIRUS; CLASS-II REGION; MAJOR HISTOCOMPATIBILITY COMPLEX; NECROSIS-FACTOR-ALPHA; ALTER PEPTIDASE ACTIVITIES; NUCLEAR TRANSLOCATION; TRANSCRIPTION FACTOR; INTERLEUKIN-8 GENE; PROTEASOME PATHWAY; HUMAN MHC;
Keywords:
respiratory syncytial virus; pulmonary inflammation; major histocompatibility complex class II locus; ABC transporter; 26S proteasome; interferon-beta alpha;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Brasier, AR Univ Texas, Med Branch, Div Endocrinol, Dept Med, MRB 8-138,301 Univ Blvd,Galveston, TX 77555 USA Univ Texas MRB 8-138,301 Univ Blvd Galveston TX USA 77555 USA
Citazione:
M. Jamaluddin et al., "IFN-beta mediates coordinate expression of antigen-processing genes in RSV-infected pulmonary epithelial cells", AM J P-LUNG, 280(2), 2001, pp. L248-L257

Abstract

Major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTLs) clear respiratory tract infections caused by the pneumovirusrespiratory syncytial virus (RSV) and also mediate vaccine-induced pulmonary injury. Herein we examined the mechanism for RSV-induced MHC class I presentation. Like infectious viruses, conditioned medium from RSV-infected cells (RSV-CM) induces naive cells to coordinately express a gene cluster encoding the transporter associated with antigen presentation 1 (TAP1) and lowmolecular mass protein (LMP) 2 and LMP7. Neutralization of RSV-CM with antibodies to interferon (IFN)-beta largely blocked TAP1/LMP2/LMP7 expression,whereas anti-interleukin-1 antibodies were without effect, and recombinantIFN-beta increased TAP1/LMP2/LMP7 expression to levels produced by RSV-CM. LMP2, LMP7, and TAP1 expression were required for MHC class I upregulationbecause the irreversible proteasome inhibitor lactacystin or transfection with a competitive TAP1 inhibitor blocked inducible class I expression. We conclude that RSV infection coordinately increases MHC class I expression and proteasome activity through the paracrine action of IFN-beta to induce expression of the TAP1/LMP2/LMP7 locus, an event that may be important in the initiation of CTL-mediated lung injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 18:04:29