期刊
SCIENCE TRANSLATIONAL MEDICINE
卷 3, 期 71, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scitranslmed.3001847
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资金
- National Institute for Health Research [DHCS/06/05/012] Funding Source: researchfish
- Medical Research Council Funding Source: Medline
- NHLBI NIH HHS [R01 HL086936, R01 HL-086936] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Department of Health [DHCS/06/05/012] Funding Source: Medline
The extracellular matrix in the lung must be destroyed for Mycobacterium tuberculosis-the agent that causes tuberculosis (TB)-to spread. The current paradigm proposes that this destruction occurs as a result of the action of proinflammatory cytokines, chemokines, immune cells, and lipids that mediate TB-associated necrosis in the lung. However, this view neglects the fact that lung matrix can only be degraded by proteases. We propose an original conceptual framework of TB immunopathology that may lead directly to treatments that involve inhibition of matrix metalloproteinase activity to hinder matrix destruction and reduce the morbidity and mortality associated with TB.
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