近日，內(nèi)蒙古醫(yī)科大學附屬醫(yī)院檢驗科鄭文琪課題組閆志老師，使用IPHASE品牌產(chǎn)品：CD4+T 細胞在《Cytokine》期刊上發(fā)表文章《Diagnostic accuracy and cellular origin of pleural fluid CXCR3 ligands for tuberculous pleural effusion》，影響因子3.8！
本論文中，評估了 CXCL9 和 CXCL11 對結(jié)核性胸腔積液(TPE)的診斷潛力，并確定了它們在 TPE 發(fā)生過程中的細胞起源和作用。我們在中國的兩個中心前瞻性地招募了未確診的胸腔積液患者。我們收集了入院時的胸腔積液，并測定了 CXCL9 和 CXCL11 的水平。采用 ROC 曲線和 DCA 評估了 CXCL9 和 CXCL11 的診斷準確性。用卡介苗(Bacillus Calmette-Guérin，BCG)處理 THP-1 細胞衍生的巨噬細胞，并采用 qRT-PCR 和 ELISA 方法測定 CXCL9 和 CXCL11。CXCL9和CXCL11對Th細胞的趨化吸引活性通過透孔試驗進行了分析。我們發(fā)現(xiàn)胸膜 CXCL9 和 CXCL11 是 TPE 的潛在診斷標志物，但其診斷準確性在老年患者中受到影響。CXCL9 和 CXCL11 可促進外周 Th 細胞向胸膜腔遷移，從而成為治療 TPE 的靶點。
摘要
Background: Pleural biomarkers represent potential diagnostic tools for tuberculous pleural effusion (TPE) due to their advantages of low cost, short turnaround time, and less invasiveness. This study evaluated the diagnostic
accuracy of two CXCR3 ligands, C-X-C motif chemokine ligand 9 (CXCL9) and CXCL11, for TPE. In addition, we investigated the cellular origins and biological roles of CXCL9 and CXCL11 in the development of TPE.
Methods: This double-blind study prospectively enrolled patients with undiagnosed pleural effusion from two centers (Hohhot and Changshu) in China. Pleural fluid on admission was obtained and levels of CXCL9 and CXCL11 were measured by an enzyme-linked immunosorbent assay (ELISA). The receiver operating character-istic (ROC) curve and the decision curve analysis (DCA) were used to evaluate their diagnostic accuracy and net benefit, respectively. THP-1 cell-derived macrophages were treated with Bacillus Calmette-Gu´erin (BCG), and quantitative real-time PCR (qRT-PCR) and ELISA were used to determine the mRNA and protein levels of CXCL9 and CXCL11. The chemoattractant activities of CXCL9 and CXCL11 for T helper (Th) cells were analyzed by a transwell assay.
Results: One hundred and fifty-three (20 TPEs and 133 non-TPEs) patients were enrolled in the Hohhot Center, and 58 (13 TPEs and 45 non-TPEs) were enrolled in the Changshu Center. In both centers, we observed increased CXCL9 and CXCL11 in TPE patients. The areas under the ROC curves (AUCs) of pleural CXCL9 and CXCL11 in the Hohhot Center were 0.70 (95 % CI: 0.55–0.85) and 0.68 (95 % CI: 0.52-0.84), respectively. In the Changshu Center, the AUCs of CXCL9 and CXCL11 were 0.96 (95 % CI: 0.92–1.00) and 0.97 (95 % CI: 0.94–1.00), respectively. The AUCs of CXCL9 and CXCL11 decreased with the advancement of age. The decision curves of CXCL9 and CXCL11 showed net benefits in both centers. CXCL9 and CXCL11 were upregulated in BCG-treated macrophages. Pleural fluid from TPE and conditioned medium from BCG-treated macrophages were chemotactic for Th cells. Anti-CXCL9 or CXCL11 neutralizing antibodies could partly block the chemotactic activity. Conclusions: Pleural CXCL9 and CXCL11 are potential diagnostic markers for TPE, but their diagnostic accuracy is compromised in elderly patients. CXCL9 and CXCL11 can promote the migration of peripheral Th cells, thus representing a therapeutic target for the treatment of TPE.
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