Sci Transl Med 23 February 2011: Vol. 3, Issue 71, p. 71ps6 : DOI: 10.1126/scitranslmed.3001847
Paul T. Elkington1,*, Jeanine M. D’Armiento2 and Jon S. Friedland1
Abstract
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.
Citation: P. T. Elkington, J. M. D’Armiento, J. S. Friedland, Tuberculosis Immunopathology: The Neglected Role of Extracellular Matrix Destruction. Sci. Transl. Med. 3, 71ps6 (2011).
http://stm.sciencemag.org/content/3/71/71ps6.abstract
Paul T. Elkington1,*, Jeanine M. D’Armiento2 and Jon S. Friedland1
Abstract
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.
Citation: P. T. Elkington, J. M. D’Armiento, J. S. Friedland, Tuberculosis Immunopathology: The Neglected Role of Extracellular Matrix Destruction. Sci. Transl. Med. 3, 71ps6 (2011).
http://stm.sciencemag.org/content/3/71/71ps6.abstract
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