Published December 2, 2013 - More info
Chronic obstructive lung disease is characterized by persistent abnormalities in epithelial and immune cell function that are driven, at least in part, by infection. Analysis of parainfluenza virus infection in mice revealed an unexpected role for innate immune cells in IL-13–dependent chronic lung disease, but the upstream driver for the immune axis in this model and in humans with similar disease was undefined. We demonstrate here that lung levels of IL-33 are selectively increased in postviral mice with chronic obstructive lung disease and in humans with very severe chronic obstructive pulmonary disease (COPD). In the mouse model, IL-33/IL-33 receptor signaling was required for
Derek E. Byers, Jennifer Alexander-Brett, Anand C. Patel, Eugene Agapov, Geoffrey Dang-Vu, Xiaohua Jin, Kangyun Wu, Yingjian You, Yael Alevy, Jean-Philippe Girard, Thaddeus S. Stappenbeck, G. Alexander Patterson, Richard A. Pierce, Steven L. Brody, Michael J. Holtzman
Original citation: J Clin Invest. 2013;123(9):3967–3982. doi:10.1172/JCI65570.
Citation for this corrigendum: J Clin Invest. 2013;123(12):5410. doi:10.1172/JCI74125.
The author list for reference 83 was incorrect. The correct reference is below.
83. Cairns JM, Dunning MJ, Ritchie ME, Russell RC, Lynch AG. BASH: a tool for managing BeadArray spatial artefacts. Bioinformatics. 2008;24(24):2921–2922.
The authors regret the error.