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 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.
Velasco-Velázquez
Marco Antonio
MA
Department of Pharmacology, School of Medicine, National Autonomous University of Mexico, Mexico City, Mexico.
Barrera
Diana
D
González-Arenas
Aliesha
A
Rosales
Carlos
C
Agramonte-Hevia
José
J
D000818:Animals; D006801:Humans; D016177:Macrophage-1 Antigen / Q000378:metabolism*; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology*; D051379:Mice; D009169:Mycobacterium tuberculosis / Q000276:immunology* / Q000472:pathogenicity*; D010587:Phagocytosis / Q000502:physiology; D014376:Tuberculosis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology
D016177:Macrophage-1 Antigen