title: Increased numbers of dendritic cells in the bronchiolar tissues of diffuse panbronchiolitis.
abstract: Dendritic cells (DCs) are potent antigen-presenting cells (APCs); they are considered to be the most important APC in the lung. Recently, the number of DCs in the large airways was demonstrated to increase in patients with atopic asthma, leading to the concept that DCs play an important role in airway inflammation. However, little is known about the distribution of lung DCs in the small airways under other pathological conditions. The aim of the present study was to examine the distribution of DCs in the bronchiolar tissues in patients with diffuse panbronchiolitis (DPB), which is a chronic inflammatory disorder of the airways histologically characterized by peribronchiolitis. We investigated the distribution of DCs in the bronchiolar tissues of the lungs in 11 patients with DPB and 7 control subjects with normal lungs using immunohistochemical methods. Marked increases in the number of CD1a(+), CD1c(+), and CD83(+) DCs were found in both the bronchiolar epithelium and submucosal tissues of patients with DPB, compared with control subjects with normal lungs. The most striking increase occurred in the number of DCs expressing CD83, a marker of mature DCs, in the submucosal tissues of patients with DPB. The increases of these positive cells in patients with DPB were more marked in the submucosal tissues than in the epithelium. The bronchiolar epithelial cells in patients with DPB strongly expressed GM-CSF protein, which is an important cytokine for the differentiation and function of DCs, suggesting that the increased local production of GM-CSF may be responsible for the accumulation and differentiation of DCs in the bronchiolar tissues of patients with DPB. These results suggest that increased DCs in the bronchiolar tissues, together with their phenotypical maturation, may play an important role in the mucosal immune response in patients with DPB through their potent antigen-presenting function.
authors.affiliation: Second Division of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Todate
authors.forename: K
authors.initials: K
authors.lastname: Chida
authors.forename: T
authors.initials: T
authors.lastname: Suda
authors.forename: S
authors.initials: S
authors.lastname: Imokawa
authors.forename: J
authors.initials: J
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Ide
authors.forename: T
authors.initials: T
authors.lastname: Tsuchiya
authors.forename: N
authors.initials: N
authors.lastname: Inui
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Asada
authors.forename: H
authors.initials: H
authors.lastname: Hayakawa
authors.forename: H
authors.initials: H
authors.lastname: Nakamura
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000096:biosynthesis; D001980:Bronchi / Q000473:pathology*; D001988:Bronchiolitis / Q000473:pathology*; D002452:Cell Count; D003713:Dendritic Cells / Q000276:immunology; D005260:Female; D006801:Humans; D008264:Macrophages; D008297:Male; D008875:Middle Aged
chemical_list: D015703:Antigens, CD