Format

Send to

Choose Destination
J Immunol. 2015 Apr 15;194(8):3962-9. doi: 10.4049/jimmunol.1403043. Epub 2015 Mar 18.

A critical role for dendritic cells in the evolution of IL-1β-mediated murine airway disease.

Author information

1
Department of Pathology, University of California, San Francisco, San Francisco, CA 94110; and.
2
Department of Medicine, University of California, San Francisco, San Francisco, CA 94110.
3
Department of Pathology, University of California, San Francisco, San Francisco, CA 94110; and stephen.nishimura@ucsf.edu.

Abstract

Chronic airway inflammation and fibrosis, known as airway remodeling, are defining features of chronic obstructive pulmonary disease and are refractory to current treatments. How and whether chronic inflammation contributes to airway fibrosis remain controversial. In this study, we use a model of chronic obstructive pulmonary disease airway disease utilizing adenoviral delivery of IL-1β to determine that adaptive T cell immunity is required for airway remodeling because mice deficient in α/β T cells (tcra(-/-)) are protected. Dendritic cells (DCs) accumulate around chronic obstructive pulmonary disease airways and are critical to prime adaptive immunity, but they have not been shown to directly influence airway remodeling. We show that DC depletion or deficiency in the crucial DC chemokine receptor ccr6 both protect from adenoviral IL-1β-induced airway adaptive T cell immune responses and fibrosis in mice. These results provide evidence that chronic airway inflammation, mediated by accumulation of α/β T cells and driven by DCs, is critical to airway fibrosis.

PMID:
25786688
PMCID:
PMC4390519
DOI:
10.4049/jimmunol.1403043
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center