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Titolo:
Utilization of CD11b knockout mice to characterize the role of complement receptor 3 (CR3, CD11b/CD18) in the growth of Mycobacterium tuberculosis inmacrophages
Autore:
Melo, MD; Catchpole, IR; Haggar, G; Stokes, RW;
Indirizzi:
Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada Univ British Columbia Vancouver BC Canada V5Z 1M9 ver, BC V5Z 1M9, Canada Univ British Columbia, Dept Pediat, Vancouver, BC V5Z 1M9, Canada Univ British Columbia Vancouver BC Canada V5Z 1M9 ver, BC V5Z 1M9, Canada Univ British Columbia, Dept Microbiol & Immunol, Vancouver, BC V5Z 1M9, Canada Univ British Columbia Vancouver BC Canada V5Z 1M9 ver, BC V5Z 1M9, Canada British Columbia Childrens Hosp, Div Infect Dis & Immunol, Vancouver, BC V6H 3V4, Canada British Columbia Childrens Hosp Vancouver BC Canada V6H 3V4H 3V4, Canada Glaxo Wellcome Res & Dev Ltd, Med Res Ctr, Dept Cell Biol, Stevenage SG1 2NY, Herts, England Glaxo Wellcome Res & Dev Ltd Stevenage Herts England SG1 2NY rts, England Glaxo Wellcome Res & Dev Ltd, Med Res Ctr, Dept Comparat Pathol, StevenageSG1 2NY, Herts, England Glaxo Wellcome Res & Dev Ltd Stevenage Herts England SG1 2NY rts, England
Titolo Testata:
CELLULAR IMMUNOLOGY
fascicolo: 1, volume: 205, anno: 2000,
pagine: 13 - 23
SICI:
0008-8749(20001010)205:1<13:UOCKMT>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
SITE-DIRECTED MUTAGENESIS; BINDING LECTIN SITE; NONOPSONIC BINDING; MURINE MACROPHAGES; MEDIATED UPTAKE; HUMAN-MONOCYTES; ALVEOLAR MACROPHAGES; STEM-CELLS; IN-VIVO; GENE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Stokes, RW BC Res Inst Childrens & Womens Hlth, Room 304,950 W 28th Ave, Vancouver, BC V5Z 4H4, Canada BC Res Inst Childrens & Womens Hlth Room 304,950 W 28th Ave Vancouver BC Canada V5Z 4H4
Citazione:
M.D. Melo et al., "Utilization of CD11b knockout mice to characterize the role of complement receptor 3 (CR3, CD11b/CD18) in the growth of Mycobacterium tuberculosis inmacrophages", CELL IMMUN, 205(1), 2000, pp. 13-23

Abstract

Using CD11b knockout mice as a source of macrophages (M phi), we show thatcomplement receptor 3 (CR3) mediates approximately 40-50% of nonopsonic binding and 50-60% of serum-mediated binding of Mycobacterium tuberculosis toresident M phi. We demonstrate that opsonic binding of M. tuberculosis to M phi is mediated by an immunoglobulin-independent, heatlabile component ofserum, in both the presence and the absence of CD11b. The survival and replication of M. tuberculosis in an in vitro M phi model and an in vivo mousemodel of infection were not significantly affected by the absence of CD11b, indicating that CR3-mediated uptake of M. tuberculosis is not a major factor in controlling the subsequent intracellular survival of the mycobacteria. However, whether a mycobacterium will gain access to the intracellular environment, and the type of M phi that the bacterium enters, is significantly affected by the presence or absence of CR3. (C) 2000 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 15:31:22