细胞因子信号转导抑制蛋白 3 和 5 有可能划定慢性鼻炎 Th 细胞的极化。

IF 2.5 3区 工程技术 Q2 BIOLOGY Yale Journal of Biology and Medicine Pub Date : 2024-06-28 eCollection Date: 2024-06-01 DOI:10.59249/HZFN2950
Babak Ghalehbaghi, Hossein Aazami, Majid Khoshmirsafa, Alireza Mohebbi, Pegah Babaheidarian, Nesa Rashidi, Kobra Mokhtarian, Reza Ahmadi, Monireh Kamali, Majid Ponour, Ayda Sanaei, Farhad Seif, Maryam Jalessi
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引用次数: 0

摘要

背景:慢性鼻窦炎(CRS)是一种炎症,分为有鼻息肉的慢性鼻窦炎(CRSwNP)和无鼻息肉的慢性鼻窦炎(CRSsNP)。Th 细胞管理着 CRS 中的炎症细胞。细胞因子信号抑制因子(SOCS)蛋白通过向 Th1、Th2 和 Th17 细胞极化,调节 Th 细胞中 Janus 激酶(JAK)-信号转导和转录激活因子(STAT)通路。本研究评估了CRS患者体内SOCS1、3、5的水平,以发现其与Th细胞的关联。研究方法在这项横断面研究中,20 名 CRSwNP 患者、12 名 CRSsNP 患者和 12 名对照组参加了研究。采用免疫组化法测定 CD4+ T 细胞的浸润情况。使用实时 PCR 评估特定转录因子和 SOCS 蛋白的表达。使用 ELISA 评估细胞因子水平。采用 Western 印迹分析法检测 SOCS 蛋白水平。结果与 CRSsNP 组和对照组相比,CRSwNP 组 SOCS3 的表达量增加(p p p p p 结论:CRSwNP 组 SOCS3 的表达量比对照组高:SOCS3和SOCS5蛋白分别负责将Th细胞极化为Th2或Th1细胞,通过调节这两种蛋白,可为CRS提供靶向疗法。JAK-STAT 通路的靶向作用涉及众多细胞,但可以仅限于 SOCS 蛋白,从而更有效地协调 Th 细胞的分化。
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Suppressor of Cytokine Signaling Proteins 3 and 5 Potentially Delineate Polarization of Th cells in Chronic Rhinosinusitis.

Background: Chronic rhinosinusitis (CRS) is an inflammatory condition classified into chronic rhinosinusitis with nasal polyps (CRSwNP) and chronic rhinosinusitis without nasal polyps (CRSsNP). Th cells manage inflammatory cells in CRS. Suppressor of Cytokine Signaling (SOCS) proteins regulate Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway in Th cells by polarizing toward Th1, Th2, and Th17 cells. This study evaluated the levels of SOCS1,3,5 in CRS patients to find associations with Th cells. Methods: In this cross-sectional study, 20 CRSwNP patients, 12 CRSsNP patients, and 12 controls participated. The infiltration of CD4+ T cells was determined using immunohistochemistry. The expression of specific transcription factors and SOCS proteins was assessed using real-time PCR. Cytokine levels were evaluated using ELISA. SOCS protein levels were investigated using western blot analysis. Results: The expression of SOCS3 increased in the CRSwNP group compared to CRSsNP and control groups (p <0.001). SOCS3 protein levels increased in the CRSwNP group compared to CRSsNP (p <0.05) and control (p <0.001) groups. Although there was a significant difference in SOCS5 expression between CRSsNP and control groups, SOCS5 protein levels were significantly different between CRSsNP and control (p <0.001) and CRSwNP (p <0.05) groups. Conclusions: Targeted therapies may be suggested for CRS by modulating SOCS3 and SOCS5 proteins that are responsible for polarization of Th cells toward Th2 or Th1 cells, respectively. JAK-STAT pathway targeting, which encompasses numerous cells, can be limited to SOCS proteins to more effectively orchestrate Th cell differentiation.

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Yale Journal of Biology and Medicine
Yale Journal of Biology and Medicine Biochemistry, Genetics and Molecular Biology-General Biochemistry,Genetics and Molecular Biology
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期刊介绍: The Yale Journal of Biology and Medicine (YJBM) is a graduate and medical student-run, peer-reviewed, open-access journal dedicated to the publication of original research articles, scientific reviews, articles on medical history, personal perspectives on medicine, policy analyses, case reports, and symposia related to biomedical matters. YJBM is published quarterly and aims to publish articles of interest to both physicians and scientists. YJBM is and has been an internationally distributed journal with a long history of landmark articles. Our contributors feature a notable list of philosophers, statesmen, scientists, and physicians, including Ernst Cassirer, Harvey Cushing, Rene Dubos, Edward Kennedy, Donald Seldin, and Jack Strominger. Our Editorial Board consists of students and faculty members from Yale School of Medicine and Yale University Graduate School of Arts & Sciences. All manuscripts submitted to YJBM are first evaluated on the basis of scientific quality, originality, appropriateness, contribution to the field, and style. Suitable manuscripts are then subject to rigorous, fair, and rapid peer review.
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