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Titolo:
Mycobacterium tuberculosis infection in complement receptor 3-deficient mice
Autore:
Hu, CG; Mayadas-Norton, T; Tanaka, K; Chan, J; Salgame, P;
Indirizzi:
Temple Univ, Sch Med, Dept Microbiol & Immunol, Philadelphia, PA 19140 USATemple Univ Philadelphia PA USA 19140 Immunol, Philadelphia, PA 19140 USA Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 h Med, Dept Pathol, Boston, MA 02115 USA Montefiore Med Ctr, Dept Pathol, Bronx, NY 10461 USA Montefiore Med Ctr Bronx NY USA 10461 r, Dept Pathol, Bronx, NY 10461 USA Montefiore Med Ctr, Dept Med, Bronx, NY 10461 USA Montefiore Med Ctr Bronx NY USA 10461 Ctr, Dept Med, Bronx, NY 10461 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 5, volume: 165, anno: 2000,
pagine: 2596 - 2602
SICI:
0022-1767(20000901)165:5<2596:MTIICR>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALVEOLAR MACROPHAGES; NONOPSONIC BINDING; ATTENUATED STRAINS; MEDIATED UPTAKE; VIRULENT; PHAGOCYTOSIS; MECHANISM; LIPOARABINOMANNAN; INTERLEUKIN-12; SUPPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Salgame, P Temple Univ, Sch Med, Dept Microbiol & Immunol, 3400 N Broad St,Kresge Room 501, Philadelphia, PA 19140 USA Temple Univ 3400 N Broad St,Kresge Room 501 Philadelphia PA USA 19140
Citazione:
C.G. Hu et al., "Mycobacterium tuberculosis infection in complement receptor 3-deficient mice", J IMMUNOL, 165(5), 2000, pp. 2596-2602

Abstract

Complement receptor type 3 (CR3) present on macrophages Is used by Mycobacterium tuberculosis as one of its major phagocytic receptors, In this study, we examined the in vivo significance of CR3-mediated phagocytosis on the pathogenesis of disease caused by M. tuberculosis. The outcome of tuberculous infection in mice deficient in the CD11b subunit of CR3 (CR3(-/-)) on a mixed 129SV and C57BL background and control wild-type counterparts was comparable with respect to survival, bacterial burden, granulomatous lesion development, and cytokine expression in the spleen and lungs. M. tuberculosisinfection was also examined in CR3(-/-) mice on C57BL/6 and BALB/c backgrounds and was found to be similar, In conclusion, our results suggest that in the absence of CR3, M. tuberculosis is able to gain entry into host cellsvia alternative phagocytic receptors and establish infection. The data also indicate that absence of CR3 does not alter disease course in either the relatively resistant C57BL/6 or the relatively susceptible BALB/c strains of mice.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 16:15:02