Utilization of CD11b knockout mice to characterize the role of complement receptor 3 (CR3, CD11b/CD18) in the growth of Mycobacterium tuberculosis in macrophages.
Cell Immunol
; 205(1): 13-23, 2000 Oct 10.
Article
en En
| MEDLINE
| ID: mdl-11078603
ABSTRACT
Using CD11b knockout mice as a source of macrophages (Mphi;), we show that complement receptor 3 (CR3) mediates approximately 40-50% of nonopsonic binding and 50-60% of serum-mediated binding of Mycobacterium tuberculosis to resident Mphi;. We demonstrate that opsonic binding of M. tuberculosis to Mphi; is mediated by an immunoglobulin-independent, heat-labile component of serum, in both the presence and the absence of CD11b. The survival and replication of M. tuberculosis in an in vitro Mphi; model and an in vivo mouse model 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 Mφ that the bacterium enters, is significantly affected by the presence or absence of CR3.
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Banco de datos:
MEDLINE
Asunto principal:
Antígeno de Macrófago-1
/
Antígenos CD18
/
Macrófagos
/
Mycobacterium tuberculosis
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Año:
2000
Tipo del documento:
Article