屋尘螨
外周血单个核细胞
免疫学
狭缝
流式细胞术
医学
发病机制
T细胞
过敏
细胞因子
过敏原
生物
免疫系统
体外
遗传学
生物化学
作者
Fumiaki Ihara,Daiju Sakurai,Syuji Yonekura,Tomohisa Iinuma,Ryoji Yagi,Toshioki Sakurai,Takashi Ito,Akira Matsuura,Yuki Morimoto,Tomoyuki Arai,Satoshi Suzuki,K. Katayama,Toshinori Nakayama,Yoshitaka Okamoto
出处
期刊:Allergy
[Wiley]
日期:2018-03-08
卷期号:73 (9): 1823-1832
被引量:75
摘要
Abstract Background Although Th2 cells are well known to play important roles in allergic diseases including allergic rhinitis ( AR ), the factors that induce and sustain the pathogenesis of AR remain unclear. The recent development of sublingual immunotherapy ( SLIT ) is expected to allow changes to the underlying pathogenesis of AR . However, which Th2 cell subsets are important in house dust mite‐induced AR ( HDM ‐ AR ), the influence of SLIT on the pathogenic Th2 cells, and the association of Th2 cell subsets with SLIT efficacy have not been clarified. Methods The cytokine production and frequency of HDM ‐reactive T‐cell subsets in peripheral blood mononuclear cells ( PBMC s) were evaluated using flow cytometry in 89 HDM ‐ AR patients (placebo [n = 43] and HDM 300 IR [n = 46]) who participated in a placebo‐controlled study of SLIT with HDM tablets. All patients provided samples both before treatment as a baseline and at the end of the 52‐week study. The PBMC s were stained with CellTrace™ Violet ( CTV ) before culture with HDM extract, and HDM ‐reactive T cells were detected as the proliferated cells with diminished CTV . Results HDM ‐reactive IL ‐5 + IL ‐13 + CD 27 − CD 161 + CD 4 + cells and ST 2 + CD 45 RO + CD 4 + cells were observed in the peripheral blood from each patient with HDM ‐ AR ; these cells significantly decreased after SLIT in the group treated with active tablets. HDM ‐reactive ST 2 + CD 45 RO + CD 4 + cells were significantly lower in active‐responders. Conclusion Allergen‐reactive ST 2 + CD 45 RO + CD 4 + cells or those combined with IL ‐5 + IL ‐13 + CD 27 − CD 161 + CD 4 + cells may be useful as markers indicating the successful treatment of SLIT . These cells may play a crucial role in the pathogenesis of AR as pathogenic memory Th2 cells.
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