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奥马珠单抗对慢性荨麻疹患者外周血 T 细胞的调节作用。

Peripheral blood T-cell modulation by omalizumab in chronic urticaria patients.

机构信息

Immunology Division, Laboratori Clinic Metropolitana Nord (LCMN), Germans Trias i Pujol University Hospital and Research Institute (IGTP), Badalona, Spain.

Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Badalona, Spain.

出版信息

Front Immunol. 2024 Aug 20;15:1413233. doi: 10.3389/fimmu.2024.1413233. eCollection 2024.

DOI:10.3389/fimmu.2024.1413233
PMID:39229257
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11368771/
Abstract

BACKGROUND

Chronic spontaneous urticaria (CSU) is a highly prevalent and difficult to manage cutaneous disease characterized by the presence of recurrent urticaria, angioedema, or both, for a period of 6 weeks or longer. One of the biological treatments used for patients with CSU with an autoimmune background and bad control of the disease is omalizumab, an anti-IgE monoclonal antibody. The understanding of the mechanism of action of this biological drug in CSU along with the identification of potential biomarkers of clinical response can be helpful in the personalized management of the disease.

OBJECTIVE

The purpose of this study was to analyze the effect of omalizumab on peripheral blood lymphocyte subpopulations in patients with CSU in order to identify potential biomarkers of treatment response.

METHODS

We analyzed 71 patients with CSU [33 under omalizumab and 38 under non-immunomodulatory drugs (treated with antihistamines; NID)] and 50 healthy controls. An exhaustive immunophenotyping of whole blood T-cell subpopulations, including naïve, central memory, effector memory, effector cells, Th1, Th2, and Th17 was performed by multiparametric flow cytometry. Moreover, in CSU patients, we analyzed markers of inflammation (ESR, DD, CRP), atopy (prick test, IgE quantification), and autoimmunity (anti-thyroid antibodies and indirect basophil activation test).To evaluate the clinical activity, the Urticaria Activity Score 7 (UAS 7) test was used.

RESULTS

In patients with CSU under treatment with omalizumab, there was a significant decrease in the percentage of naïve and an increase in the percentage of central memory CD4 T cells as well as a decrease in the percentage of naïve and increase in the percentage of effector CD8 T-cell subsets. Moreover, patients under treatment with omalizumab had higher percentages of Th1 and Th2 cells than patients under treatment with NID.

CONCLUSION

The immune monitoring of T-cell subpopulations in patients with CSU starting omalizumab, may be a useful strategy to analyze treatment response in the clinical practice.

摘要

背景

慢性自发性荨麻疹(CSU)是一种高度流行且难以治疗的皮肤疾病,其特征为反复发作的荨麻疹、血管性水肿或两者兼有,持续时间为 6 周或更长时间。对于自身免疫背景和疾病控制不佳的 CSU 患者,一种生物治疗方法是奥马珠单抗,一种抗 IgE 单克隆抗体。了解这种生物药物在 CSU 中的作用机制以及鉴定潜在的临床反应生物标志物,有助于疾病的个体化管理。

目的

本研究旨在分析奥马珠单抗对 CSU 患者外周血淋巴细胞亚群的影响,以确定潜在的治疗反应生物标志物。

方法

我们分析了 71 例 CSU 患者[33 例接受奥马珠单抗治疗,38 例接受非免疫调节药物(抗组胺治疗;NID)治疗]和 50 名健康对照者。采用多参数流式细胞术对全血 T 细胞亚群进行了详尽的免疫表型分析,包括幼稚细胞、中央记忆细胞、效应记忆细胞、效应细胞、Th1、Th2 和 Th17。此外,在 CSU 患者中,我们分析了炎症标志物(ESR、DD、CRP)、过敏症(划痕试验、IgE 定量)和自身免疫(甲状腺抗体和间接嗜碱性粒细胞激活试验)。为了评估临床疗效,采用荨麻疹活动评分 7 项(UAS7)测试。

结果

在接受奥马珠单抗治疗的 CSU 患者中,幼稚细胞的比例显著下降,中央记忆 CD4 T 细胞的比例增加,幼稚细胞的比例下降,效应 CD8 T 细胞亚群的比例增加。此外,与接受 NID 治疗的患者相比,接受奥马珠单抗治疗的患者 Th1 和 Th2 细胞的比例更高。

结论

对开始接受奥马珠单抗治疗的 CSU 患者 T 细胞亚群进行免疫监测,可能是分析临床疗效的一种有用策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/68e8df1a0e82/fimmu-15-1413233-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/4711bbdeac08/fimmu-15-1413233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/61c6004a8425/fimmu-15-1413233-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/1aa8d0398e96/fimmu-15-1413233-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/05d3e8f601cd/fimmu-15-1413233-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/4745cf2031e5/fimmu-15-1413233-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/68e8df1a0e82/fimmu-15-1413233-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/4711bbdeac08/fimmu-15-1413233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/61c6004a8425/fimmu-15-1413233-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/1aa8d0398e96/fimmu-15-1413233-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/05d3e8f601cd/fimmu-15-1413233-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/4745cf2031e5/fimmu-15-1413233-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b7/11368771/68e8df1a0e82/fimmu-15-1413233-g006.jpg

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