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

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

  • Am J Respir Cell Mol Biol. 2014 May;50(5):985-94. doi: 10.1165/rcmb.2013-0342OC.
Lynne A Murray 1 Huilan Zhang Sameer R Oak Ana Lucia Coelho Athula Herath Kevin R Flaherty Joyce Lee Matt Bell Darryl A Knight Fernando J Martinez Matthew A Sleeman Erica L Herzog Cory M Hogaboam
Affiliations

Affiliation

  • 1 1 MedImmune Ltd, Cambridge, United Kingdom.
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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