The role of CCL22/macrophage-derived chemokine in allergic rhinitis

Dendritic cells (DCs) are considered to be the most powerful antigen-presenting cells (APCs). DCs are thought to be associated with Th1 or Th2 polarization and with polarization-induced disease such as atopic dermatitis, asthma and allergic rhinitis, but its mechanism is not well known. In this stud...

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Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 125(2007), 3 vom: 01. Dez., Seite 291-8
1. Verfasser: Yanai, Mitsuru (VerfasserIn)
Weitere Verfasser: Sato, Keisuke, Aoki, Naoko, Takiyama, Yumi, Oikawa, Kensuke, Kobayashi, Hiroya, Kimura, Shoji, Harabuchi, Yasuaki, Tateno, Masatoshi
Format: Aufsatz
Sprache:English
Veröffentlicht: 2007
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Antigens, CD CCR4 protein, human Chemokine CCL22 Chemokines RNA, Messenger Receptors, CCR4
Beschreibung
Zusammenfassung:Dendritic cells (DCs) are considered to be the most powerful antigen-presenting cells (APCs). DCs are thought to be associated with Th1 or Th2 polarization and with polarization-induced disease such as atopic dermatitis, asthma and allergic rhinitis, but its mechanism is not well known. In this study, we analyzed the mRNA expression of DCs between birch pollen allergic rhinitis and healthy controls by using cDNA array. We found that the expressions of CCL22/macrophage-derived chemokine (MDC) differed significantly. We also revealed that CCL22/MDC production was higher in patients than in healthy donors. By chemotaxis assay, CCL22/MDC can enhance the migration of patient's T cells rather than those of healthy controls. Surface marker analysis of migrated cells revealed that the most of migrated cells expressed CCR4, which were considered to be Th2 cells. Furthermore, CD1a(+) CD83(+) cells located in the nasal mucosa expressed CCL22/MDC in vivo. To the best of our knowledge, this is the first report clearly indicating the role of CCL22/MDC in allergic rhinitis
Beschreibung:Date Completed 22.01.2008
Date Revised 23.11.2007
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035