2026-11-092026-11-09https://scholars.csmu.edu.tw/handle/123456789/38744Autoimmune and allergy are both diseases resulting from immunologic dysregulation. Recently, increasing evidences showed intimate linkage between autoimmune and allergy, including clinical findings about systemic lupus erythematosus (SLE) patients may suffer from asthma simultaneously. On the contrary, asthma patients may also suffer from SLE. However, the immunologic mechanisms between autoimmune and allergy are still unclear. Among the inhalant allergens inducing asthma, house dust mite (HDM), mainly including Dermatophagoides pteronyssinus and Dermatophagoides farinae, is an important source. Previous studies have showed that group I- and II-HDM allergens are both reported as major allergens, but few investigations for allergenic characterization of group-II allergens. Our preliminary study showed that group-II HDM allergen, Der f 2 (DF2), inhibited the clustering and proliferation of autoreactive B lymphocyte. We also found that Der f 2 influenced the protein expression of airway epithelial cells. For these reasons, we intently investigate the molecular mechanisms for DF2-induced apoptosis in autoreactive B lymphocyte and airway epithelium. After that, we will compare the varied mechanisms induced by DF2, group-I and group-II HDM allergens. The aim of the study is trying to comprehensively understand the effects of group-I, -II and -III HDM allergens on airway epithelium cell line A549 and autoreactive B lymphocyte. To achieve the purpose, we use a combination of proteomic and immunomic approach. This investigation not only further understand the allergenic characterization of HDM allergens, but also greatly improve our realization on allergen-induced apoptosis in autoreactive B lymphocyte. Finally, we may develop novel therapeutic treatments by new targets found in this study.自體免疫疾病與過敏性氣喘為皆為免疫調控異常之重大疾病之一，越來越多的研究顯示兩 者之間有密切的關聯。此外臨床證據也顯示，過敏病人中可能會同時發生自體免疫疾病， 反之亦然，自體免疫病人中也有可能同時罹患過敏疾病，但是其免疫致病機制的關連性仍 不清楚。在過敏原誘發的的氣喘中，塵螨為最重要的室內過敏來源，過去的研究顯示第1、 2 群過敏原皆為主要過敏原，但是第2 群過敏原的致敏機制仍存在許多未知之處。 我們先前的研究發現，第 2 群塵螨過敏原Der f 2 會抑制自體反應性B 淋巴球的聚集與增 生，同時也會改變呼吸道上皮細胞的蛋白質表現。因此在本研究中，我們企圖更進一步地 分析Der f 2 對呼吸道上皮細胞與自體反應性B 淋巴球產生細胞凋亡的分子作用機制，並 同時比較具有不同生化特性的第1、2、3 群塵螨過敏原之分子作用機制的異同。 本計畫的目的，在於應用蛋白體與免疫體研究法，綜觀性地分析探討第 2 群與第1、3 群 過敏原，對呼吸道表皮細胞，以及自體反應性B 淋巴球的分子作用機制。本研究不僅可 以更深入地瞭解塵螨過敏原的致病機制，同時也進一步瞭解過敏原誘發B 淋巴球細胞凋 亡的機制與相關訊息傳導，更可以從相關的免疫分子機制中發展新的自體免疫治療標的。自體免疫氣喘塵螨過敏紅斑性狼瘡autoimmuneasthmahousedust miteallergysystemic lupus erythematosusProject