Abstract
Apoptosis is a physiological programmed cell death process whose dysregulation plays an important role in different human infectious diseases. An increasing number of intracellular pathogens are known to induce target cell apoptosis, while some other parasites inhibit it. Unlike necrosis, apoptosis is a silent immunological event occurring without inflammation. Infection-induced target cell apoptosis may be a successful strategy to eliminate pathogens and assure host survival. Conversely, apoptosis inhibition could represent an adaptive mechanism for pathogen survival, while it may be beneficial for the host to initiate an effective immune response. The worldwide increase in tuberculosis has stimulated more research aimed at defining the interaction between Mycobacterium tuberculosis and the immune system. M. tuberculosis possesses sophisticated strategies to circumvent its fate within target monocytic cells. Apoptosis of alveolar macrophages and monocytes has been described as a consequence of M. tuberculosis infection. Moreover, the observation that mycobacterial lipoproteins activate macrophages through Toll-like receptor (TLR) 2 suggests that innate immune receptors contribute to defence against M. tuberculosis. There is evidence that TLR-induced apoptosis modulates inflammation and immune activation during M. tuberculosis infection. Finally, the role of apoptotic-infected cells as a source of microbial antigens for cross-priming of effector T-cells is also discussed.
| Original language | English |
|---|---|
| Pages (from-to) | 375-383 |
| Number of pages | 9 |
| Journal | International Journal of Tuberculosis and Lung Disease |
| Volume | 9 |
| Issue number | 4 |
| Publication status | Published - Apr 2005 |
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Keywords
- Apoptosis
- Macrophages
- Monocytes
- Mycobacteria
- Tuberculosis
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
Cite this
Role of mycobacteria-induced monocyte/macrophage apoptosis in the pathogenesis of human tuberculosis. / Bocchino, Marialuisa; Galati, D.; Sanduzzi, A.; Colizzi, V.; Brunetti, E.; Mancino, G.
In: International Journal of Tuberculosis and Lung Disease, Vol. 9, No. 4, 04.2005, p. 375-383.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of mycobacteria-induced monocyte/macrophage apoptosis in the pathogenesis of human tuberculosis
AU - Bocchino, Marialuisa
AU - Galati, D.
AU - Sanduzzi, A.
AU - Colizzi, V.
AU - Brunetti, E.
AU - Mancino, G.
PY - 2005/4
Y1 - 2005/4
N2 - Apoptosis is a physiological programmed cell death process whose dysregulation plays an important role in different human infectious diseases. An increasing number of intracellular pathogens are known to induce target cell apoptosis, while some other parasites inhibit it. Unlike necrosis, apoptosis is a silent immunological event occurring without inflammation. Infection-induced target cell apoptosis may be a successful strategy to eliminate pathogens and assure host survival. Conversely, apoptosis inhibition could represent an adaptive mechanism for pathogen survival, while it may be beneficial for the host to initiate an effective immune response. The worldwide increase in tuberculosis has stimulated more research aimed at defining the interaction between Mycobacterium tuberculosis and the immune system. M. tuberculosis possesses sophisticated strategies to circumvent its fate within target monocytic cells. Apoptosis of alveolar macrophages and monocytes has been described as a consequence of M. tuberculosis infection. Moreover, the observation that mycobacterial lipoproteins activate macrophages through Toll-like receptor (TLR) 2 suggests that innate immune receptors contribute to defence against M. tuberculosis. There is evidence that TLR-induced apoptosis modulates inflammation and immune activation during M. tuberculosis infection. Finally, the role of apoptotic-infected cells as a source of microbial antigens for cross-priming of effector T-cells is also discussed.
AB - Apoptosis is a physiological programmed cell death process whose dysregulation plays an important role in different human infectious diseases. An increasing number of intracellular pathogens are known to induce target cell apoptosis, while some other parasites inhibit it. Unlike necrosis, apoptosis is a silent immunological event occurring without inflammation. Infection-induced target cell apoptosis may be a successful strategy to eliminate pathogens and assure host survival. Conversely, apoptosis inhibition could represent an adaptive mechanism for pathogen survival, while it may be beneficial for the host to initiate an effective immune response. The worldwide increase in tuberculosis has stimulated more research aimed at defining the interaction between Mycobacterium tuberculosis and the immune system. M. tuberculosis possesses sophisticated strategies to circumvent its fate within target monocytic cells. Apoptosis of alveolar macrophages and monocytes has been described as a consequence of M. tuberculosis infection. Moreover, the observation that mycobacterial lipoproteins activate macrophages through Toll-like receptor (TLR) 2 suggests that innate immune receptors contribute to defence against M. tuberculosis. There is evidence that TLR-induced apoptosis modulates inflammation and immune activation during M. tuberculosis infection. Finally, the role of apoptotic-infected cells as a source of microbial antigens for cross-priming of effector T-cells is also discussed.
KW - Apoptosis
KW - Macrophages
KW - Monocytes
KW - Mycobacteria
KW - Tuberculosis
UR - http://www.scopus.com/inward/record.url?scp=17144415540&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=17144415540&partnerID=8YFLogxK
M3 - Article
C2 - 15830742
AN - SCOPUS:17144415540
VL - 9
SP - 375
EP - 383
JO - International Journal of Tuberculosis and Lung Disease
JF - International Journal of Tuberculosis and Lung Disease
SN - 1027-3719
IS - 4
ER -