Th17 immunity in patients with allergic asthma.
BACKGROUND
Allergic asthma is an inflammatory disease regulated by the T helper (Th) cells. The Th1/Th2 imbalance has been well documented in the pathogenesis of allergic asthma. Recently, Th17 cells have been found to participate in the development of allergic asthma in animals. However, whether Th17 immunity contributes to the systemic immune responses in allergic asthmatic patients is unclear.


METHODS
Peripheral blood mononuclear cells were isolated from allergic asthmatics (n = 29) and healthy controls (n = 12). The frequencies of Th1, Th2 and Th17 cells were analyzed by flow cytometry. The related cytokine (IFN-gamma, IL-4, IL-17, IL-22, IL-23 and IL-25) concentrations in plasma and culture supernatants were measured by enzyme-linked immunosorbent assay and Luminex. The level of retinoic acid-related orphan receptor gammat (RORgammat), a key transcription factor controlling Th17 differentiation, was examined by real-time quantitative polymerase chain reaction.


RESULTS
The percentages of Th2 and Th17 cells as well as the concentrations of Th2- and Th17-related cytokines were higher in allergic asthmatics than those in healthy controls; some patients were even treated with inhaled glucocorticoid. The percentages of Th17 cells as well as the plasma concentrations of IL-17 and IL-22 tended to increase with the severity of the disease, while the IL-25 level was elevated in mild patients. A parallel elevation of IL-17 and IL-23 concentrations and an increase in RORgammat level were found in allergic asthmatics.


CONCLUSIONS
Our results suggest that besides predominant Th2 immunity, abnormal Th17 immunity may be also involved in the pathogenesis of allergic asthma.
Department of Respiratory Medicine, Zhongnan Hospital and Department of Respiratory Medicine, Renmin Hospital, Wuhan, China.
Yang
Y
Zhao
Jiong
J
Yang
Ya-Dong
YD
Gao
Wei
W
Guo
D000328:Adult; D001249:Asthma / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D002469:Cell Separation; D002478:Cells, Cultured; D018450:Disease Progression; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D020381:Interleukin-17 / Q000097:blood* / Q000235:genetics / Q000276:immunology; D053759:Interleukin-23 / Q000097:blood / Q000235:genetics / Q000276:immunology; D007378:Interleukins / Q000097:blood / Q000235:genetics / Q000276:immunology; D008297:Male; D008875:Middle Aged; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015533:Transcriptional Activation; D000097043:Interleukin-22
D020381:Interleukin-17; D053759:Interleukin-23; D007378:Interleukins; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D000097043:Interleukin-22