医学
间质性肺病
免疫学
支气管肺泡灌洗
类风湿性关节炎
免疫系统
趋化因子
细胞因子
发病机制
结缔组织病
关节炎
肺
抗体
自身免疫性疾病
内科学
作者
Juan Chen,Shuling Song,Yongliang Liu,Dehao Liu,Yihua Lin,Shuping Ge,Dana P. Ascherman
标识
DOI:10.1111/1756-185x.13316
摘要
Previous analysis of comparative anti-citrullinated heat shock protein 90 (citHSP90) antibody profiles between bronchoalveolar lavage fluid and serum indicates that the lung plays a direct role in shaping the immune repertoire of rheumatoid arthritis-associated interstitial lung disease (RA-ILD).To address the contribution of citHSP90β-specific T cells in this process, we evaluated in vitro cytokine responses to citHSP90β in RA patients with different stages of ILD as well as in controls with non-RA connective tissue disease-associated ILD (CTD-ILD). Cultures derived from whole blood were individually stimulated with HSP90β, citHSP90β, citrullinated BSA, or no antigen. The concentrations of 13 cytokines and chemokines in the plasma supernatant were then measured using Luminex xMAP technology.CitHSP90β induced significantly higher levels of interferon-γ (IFN-γ) levels in RA-ILD (interstitial lung abnormalities = 2 + 3) groups compared to the RA-no ILD group (P = 0.01), but did not stimulate the production of other cytokines (P > 0.05). Furthermore, citHSP90β did not stimulate the production of IFN-γ or other cytokines in those individuals with non-RA CTD-ILD.Overall, the production of IFN-γ by T cells stimulated with citHSP90β demonstrates a bias toward TH1 immune responses that are likely involved in the pathogenesis of RA-ILD.
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