Macrophage--Mycobacterium tuberculosis interactions: role of complement receptor 3.

Abstract:

:Tuberculosis is the leading infectious disease in the world. Mycobacterium tuberculosis, the causal agent of this disease, invades macrophages and can replicate inside them. Because invasion of macrophages is a critical step for establishing a mycobacterial infection, there is much interest in understanding the mechanisms for M. tuberculosis entry into macrophages. Complement receptor 3 (CR3) is a heterodimeric surface receptor with multiple binding sites, which can mediate complement-opsonized as well as nonopsonic entrance of M. tuberculosis into macrophages. Here, we describe and discuss the role of CR3 in macrophage[bond]M. tuberculosis interactions. The actual information suggests that CR3 mediates a substantial amount of M. tuberculosis binding to macrophages, but CR3 is not related to the mechanisms that allow mycobacteria to survive and replicate intracellularly. Understanding the mechanisms of macrophage[bond]M. tuberculosis interaction will help developing more effective methods to prevent and treat tuberculosis in the future.

journal_name

Microb Pathog

journal_title

Microbial pathogenesis

authors

Velasco-Velázquez MA,Barrera D,González-Arenas A,Rosales C,Agramonte-Hevia J

doi

10.1016/s0882-4010(03)00099-8

subject

Has Abstract

pub_date

2003-09-01 00:00:00

pages

125-31

issue

3

eissn

0882-4010

issn

1096-1208

pii

S0882401003000998

journal_volume

35

pub_type

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