Human macrophages represent the first line of defense for the containment of Mycobacterium tuberculosis infection. After phagocytosis, macrophages express activation surface markers and produce proinflammatory cytokines and chemokines whose main role is to control pathogen spreading by recruiting peripheral lymphocytes and monocytes at the site of inflammation. However, in the case of a concomitant human immunodeficiency virus (HIV) infection, these signals strongly enhance the susceptibility to viral infection both at the viral entry and replication levels. Under these conditions, viral expansion extends beyond tissue macrophages to T cells and vice-versa, according to the emerging viral phenotype. In absence of an efficient immune response, Mycobacterium tuberculosis can replicate in macrophages in an uncontrolled fashion culminating in macrophage death by apoptosis. As a consequence, a more severe form of immunedepression, involving both innate and specific immune responses, could be responsible for both ematogenous mycobacterial dissemination and extrapulmonary form of tuberculosis in HIV-infected patients.

Mariani, F., Goletti, D., Ciaramella, A., Martino, A., Colizzi, V., Fraziano, M. (2001). Macrophage response to Mycobacterium tuberculosis during HIV infection: relationships between macrophage activation and apoptosis. CURRENT MOLECULAR MEDICINE, 1(2), 209-216.

Macrophage response to Mycobacterium tuberculosis during HIV infection: relationships between macrophage activation and apoptosis

COLIZZI, VITTORIO;FRAZIANO, MAURIZIO
2001-05-01

Abstract

Human macrophages represent the first line of defense for the containment of Mycobacterium tuberculosis infection. After phagocytosis, macrophages express activation surface markers and produce proinflammatory cytokines and chemokines whose main role is to control pathogen spreading by recruiting peripheral lymphocytes and monocytes at the site of inflammation. However, in the case of a concomitant human immunodeficiency virus (HIV) infection, these signals strongly enhance the susceptibility to viral infection both at the viral entry and replication levels. Under these conditions, viral expansion extends beyond tissue macrophages to T cells and vice-versa, according to the emerging viral phenotype. In absence of an efficient immune response, Mycobacterium tuberculosis can replicate in macrophages in an uncontrolled fashion culminating in macrophage death by apoptosis. As a consequence, a more severe form of immunedepression, involving both innate and specific immune responses, could be responsible for both ematogenous mycobacterial dissemination and extrapulmonary form of tuberculosis in HIV-infected patients.
mag-2001
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/04 - PATOLOGIA GENERALE
English
Con Impact Factor ISI
Apoptosis; Tuberculosis; HIV Infections; Macrophage Activation; Macrophages; Mycobacterium tuberculosis; Immunity, Cellular; HIV; Disease Susceptibility; Humans
Mariani, F., Goletti, D., Ciaramella, A., Martino, A., Colizzi, V., Fraziano, M. (2001). Macrophage response to Mycobacterium tuberculosis during HIV infection: relationships between macrophage activation and apoptosis. CURRENT MOLECULAR MEDICINE, 1(2), 209-216.
Mariani, F; Goletti, D; Ciaramella, A; Martino, A; Colizzi, V; Fraziano, M
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/15437
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