Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases

  • E.P. Schmidt
    Program in Translational Lung Research, Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado at Denver, School of Medicine.
  • R.M. Tuder
    Program in Translational Lung Research, Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado at Denver, School of Medicine.

書誌事項

公開日
2010-01
権利情報
  • http://journals.sagepub.com/page/policies/text-and-data-mining-license
DOI
  • 10.4137/jcd.s5375
公開者
SAGE Publications

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説明

<jats:p>Apoptosis is an important contributor to the pathophysiology of lung diseases such as acute lung injury (ALI) and chronic obstructive pulmonary disease (COPD). Furthermore, the cellular environment of these acute and chronic lung diseases favors the delayed clearance of apoptotic cells. This dysfunctional efferocytosis predisposes to the release of endogenous ligands from dying cells. These so-called damage-associated molecular patterns (DAMPs) play an important role in the stimulation of innate immunity as well as in the induction of adaptive immunity, potentially against autoantigens. In this review, we explore the role of apoptosis in ALI and COPD, with particular attention to the contribution of DAMP release in augmenting the inflammatory response in these disease states.</jats:p>

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