https://scholars.lib.ntu.edu.tw/handle/123456789/416263
標題: | Antigen-driven bystander effect accelerates epicutaneous sensitization with a new protein allergen | 作者: | LI-FANG WANG JAU-SHIUH CHEN Hsu, Chih-Jung Liu, Ching-Yi Yu, Jhang-Sian SHI-CHUEN MIAW |
公開日期: | 6-三月-2009 | 出版社: | BMC | 卷: | 16 | 期: | 1 | 來源出版物: | Journal of biomedical science | 摘要: | Exposure to protein allergen epicutaneously, inducing a Th2-dominant immune response, sensitizes the host to the development of atopic disease. Antigen-driven bystander effect demonstrates that polarized T cells could instruct naïve T cells to differentiate into T cells with similar phenotype. In this study, we aimed to determine the contribution of antigen-driven bystander effect on epicutaneous sensitization with a newly introduced protein allergen. BALB/c mice were immunized intraperitoneally with BSA emulsified in alum, known to induce a Th2 response, three weeks before given BSA and OVA epicutaneously. Lymph node cells from these mice restimulated with OVA secreted higher levels IL-4, IL-5 and IL-13 as compared with cells from mice without BSA immunization. In addition, BALB/c mice immunized subcutaneously with BSA emulsified in complete Freund's adjuvant, known to induce a Th1-predominant response, also induced higher Th1 as well as Th2 cytokine response when restimulated with OVA as compared with mice without immunization. We demonstrated that subcutaneous immunization with BSA in CFA induced Th2 as well as Th1 response. The threshold of epicutaneous sensitization to OVA was also reduced, possibly due to increased expressions of IL-4 and IL-10 in the draining lymph nodes during the early phase of sensitization. In conclusion, antigen-driven bystander effect, whether it is of Th1- or Th2-predominant nature, can accelerate epicutaneous sensitization by a newly introduced protein allergen. These results provide a possible explanation for mono- to poly-sensitization spread commonly observed in atopic children. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-65949095628&doi=10.1186%2f1423-0127-16-28&partnerID=40&md5=456312b089238026b62048847d6c9493 https://scholars.lib.ntu.edu.tw/handle/123456789/416263 |
ISSN: | 1021-7770 | DOI: | 10.1186/1423-0127-16-28 |
顯示於: | 免疫學研究所 |
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