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

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 corriplement-opsonized as well as nonopsonic entrance of M. tuberculosis into macrophages. Here, we describe and discuss the role of CR3 in macrophage-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-M. tuberculosis interaction will help developing more effective methods to prevent and treat tuberculosis in the future. (C) 2003 Elsevier Ltd. All rights reserved.