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      Targeting interleukin-13 with tralokinumab attenuates lung fibrosis and epithelial damage in a humanized SCID idiopathic pulmonary fibrosis model.

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          Abstract

          The aberrant fibrotic and repair responses in the lung are major hallmarks of idiopathic pulmonary fibrosis (IPF). Numerous antifibrotic strategies have been used in the clinic with limited success, raising the possibility that an effective therapeutic strategy in this disease must inhibit fibrosis and promote appropriate lung repair mechanisms. IL-13 represents an attractive target in IPF, but its disease association and mechanism of action remains unknown. In the present study, an overexpression of IL-13 and IL-13 pathway markers was associated with IPF, particularly a rapidly progressive form of this disease. Targeting IL-13 in a humanized experimental model of pulmonary fibrosis using tralokinumab (CAT354) was found to therapeutically block aberrant lung remodeling in this model. However, targeting IL-13 was also found to promote lung repair and to restore epithelial integrity. Thus, targeting IL-13 inhibits fibrotic processes and enhances repair processes in the lung.

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          Author and article information

          Journal
          Am. J. Respir. Cell Mol. Biol.
          American journal of respiratory cell and molecular biology
          1535-4989
          1044-1549
          May 2014
          : 50
          : 5
          Affiliations
          [1 ] 1 MedImmune Ltd, Cambridge, United Kingdom.
          Article
          10.1165/rcmb.2013-0342OC
          24325475
          9b6c6149-157d-4074-a5a1-e596955b3105
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