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Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation
Published on: July 23, 2012
Increase of dendritic cells of type 2 (DC2) by altered response to IL-4 in atopic patients
Y Uchida1, K Kurasawa, H Nakajima
1Department of Internal Medicine II, Chiba University School of Medicine, Chiba City, Japan.
Background:
Recent studies have shown that there are 2 dendritic cell subpopulations, DC1 and DC2, which induce T(H)1 and T(H)2 cell differentiation in vitro, respectively.
Objective:
The purpose of this study was to determine whether there exists a deviation of DC1 and DC2 subsets and to investigate their functional abnormalities in T(H)2 cell-mediated atopic diseases.
Methods:
We analyzed the frequencies of DC1 (CD11c(+)CD123(-)) and DC2 (CD11c(-)CD123(+)) cells in peripheral blood of atopic patients; we also studied the responses of DC2 cells from atopic patients to IL-3 and IL-4 for their survival.
Results:
DC2 cells but not DC1 cells were significantly increased in peripheral blood of atopic patients in comparison with that of healthy subjects. DC2 cell numbers were positively correlated with serum IgE levels and blood eosinophil counts, the increase of which reflects T(H)2-type immune response in atopic diseases. IL-4 inhibited IL-3-induced survival of DC2 cells from healthy controls, but IL-4 failed to suppress the IL-3-induced survival of DC2 cells from atopic patients. Furthermore, IL-4 alone enhanced the survival of DC2 cells from atopic patients but not from healthy controls. However, no significant differences were found in the expression levels of activation/maturation markers on DC2 cells between atopic patients and healthy controls.
Conclusion:
These results indicate that DC2 cells are preferentially increased in atopic patients in correlation with the state of atopic allergy and that DC2 cells in atopic patients, unlike those in healthy subjects, exhibit altered responses to IL-4 for survival, suggesting that DC2 cells in atopic patients might contribute to the enhanced T(H)2 cell differentiation in atopic diseases.
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