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Unexpected role of dendritic cells in pulmonary fibrosis
  1. Jeoung-Sook Shin
  1. Microbiology and Immunology, University of California San Francisco, San Francisco, California, USA
  1. Correspondence to Dr Jeoung-Sook Shin, Microbiology and Immunology, University of California San Francisco, San Francisco, CA 94143, USA; Jeoung-Sook.Shin{at}ucsf.edu

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Pulmonary fibrosis is one of the most devastating diseases in which scars are formed in the lungs in a progressive and non-reversible fashion resulting in breathlessness and respiratory failure. Some treatments may improve symptoms or slow progression of the disease, but the benefits are temporary. Lung transplantation can be an option for treatment but involves serious complications, such as rejection and infection. Therefore, the development of a new treatment is in urgent need.

Past studies have shown that idiopathic pulmonary fibrosis (IPF) is associated with infiltration of lungs by dendritic cells (DCs). DCs are best known for their role in bridging innate and adaptive immunity. They reside in peripheral tissues, capture foreign antigens, produce inflammatory cytokines and present antigens to antigen-specific T lymphocytes inducing antigen-specific immune responses.1 Interestingly, an immunohistochemical analysis has shown that lungs of patients with IPF were associated with lymphoid aggregates and that these aggregates were enriched with DCs.2 Some other studies using flow cytometry have reported a significant increase in the frequency of DCs in the lungs and the bronchial lavage fluid in patients with IPF.3 4 These findings have raised a possibility that DC’s immune-stimulatory activity may play a significant role in the progression of pulmonary fibrosis.

The association of DCs with pulmonary fibrosis has been also observed in animal models. Intratracheal challenge of mice with bleomycin induced severe fibrosis in the lungs and the fibrosis was …

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Footnotes

  • Contributors J-SS is the sole contributor.

  • Funding This study was funded by the UCSF Sandler Asthma Basic Research Center.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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