Amanda T. Goodwin, Paul W. Noble, Amanda L. Tatler
European Respiratory Journal 2022 60: 2201748; DOI: 10.1183/13993003.01748-2022
Extract
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease characterised by the irreversible replacement of normal lung parenchyma with stiff scar tissue. The prognosis of IPF is very poor, with a median survival worse than many cancers at 2–3 years, and this condition is associated with increasing incidence and mortality rates worldwide [1–4]. Therefore, work to understand the key cells and molecular pathways that drive IPF is essential to identify new therapies for this devastating disease.
Recent work has shown that there are increased plasma cells in IPF and reducing plasma cell numbers can reduce experimental lung fibrosis. This editorial discusses the current knowledge surrounding the role of plasma cells and B-cells in IPF. https://bit.ly/3BQk53K
Footnotes
-
Conflict of interest: A.T. Goodwin has received research funding from an Asthma + Lung UK Malcolm Weallens Pulmonary Fibrosis grant and a Medical Research Council clinical training fellowship, in addition to conference travel grants from the British Association for Lung Research and the British Thoracic Society. P.W. Noble sits on the scientific advisory boards of Pliant Therapeutics and Lasson Therapeutics; he has received prior honoraria payments from Boehringer Ingelheim and Genentech/Roche and owns stocks in Pliant Therapeutics. A.L. Tatler is a co-investigator on an MRC Programme Grant and a Cystic Fibrosis Foundation project grant; additionally, she acts as a consultant to Pliant Therapeutics and Accession Therapeutics; she has received honoraria from the Universities of Edinburgh, Southampton and Hull (in the past three years) for PhD examination services and speaker fees from the Australasian Rare Lung Disease Conference in 2021.
- Received September 13, 2022.
- Accepted September 17, 2022.
- Copyright ©The authors 2022. For reproduction rights and permissions contact permissions@ersnet.org
