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白细胞介素-25通过白细胞介素-17RB受体增强2型炎症中的B细胞反应。

IL-25 Enhances B Cell Responses in Type 2 Inflammation Through IL-17RB Receptor.

作者信息

Abdu Semah, Xia Jiao, Yuan Huihui, Tan Tiak Ju, Layhadi Janice A, Shamji Mohamed H, McKenzie Andrew N J, Haloob Nora, Hopkins Claire, Woszczek Grzegorz, Till Stephen J

机构信息

School of Immunology and Microbial Sciences, King's College London, London, UK.

King's Centre for Lung Health, King's College London, London, UK.

出版信息

Allergy. 2025 Apr;80(4):965-975. doi: 10.1111/all.16472. Epub 2025 Jan 19.

DOI:10.1111/all.16472
PMID:39829150
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11969324/
Abstract

BACKGROUND

Alarmin cytokine IL-25 promotes type 2 inflammatory responses in disorders such as asthma and chronic rhinosinusitis with nasal polyps (CRSwNP) and known targets include ILC2 and Th2 cells. However, other cellular targets for IL-25 remain poorly defined.

OBJECTIVE

To investigate induction and expression of IL-25 receptor (IL-17RB) by B cells and evaluate responsiveness of IL-17RB-expressing B cells to IL-25 in vitro.

METHODS

IL-17RB expression, regulation and function on B cells were evaluated in peripheral blood-derived B cells by flow cytometry and RT-PCR, including in response to IgE-inducing stimuli (anti-CD40 mAb and IL-4). Single-cell RNA sequencing was used to compare IL-17RB+ and IL-17RB-activated peripheral blood-derived B cells. To evaluate B cell IL-17RB expression within type 2 inflamed tissue, B cells were compared from nasal polyps, control turbinate tissue and matched peripheral blood.

RESULTS

Activation of B cells with anti-CD40 and IL-4 increased IL-17RB expression at both protein and mRNA level, which was further upregulated by IL-25. B cells induced to express IL-17RB responded to IL-25 with enhanced antibody production. Single-cell RNA-sequencing showed that IL17RB+ activated B cells expressed higher levels of IGHE, CCL17 and CCL22 compared to IL17RB- B cells. B cells from nasal polyp tissue expressed higher levels of surface IL-17RB compared with control tissue, correlating with patient-reported CRSwNP severity (SNOT-22).

CONCLUSION

Peripheral blood B cells activated under IgE-inducing conditions express surface IL-17RB, and tissue IL-17RB+ B cells are increased in type 2 inflammation. IL-17RB+ cells have a distinct transcriptional profile and respond to IL-25 with enhanced antibody production, highlighting the IL-25/IL-17RB pathway as a potential therapeutic target for CRSwNP and other type 2 inflammatory disorders.

摘要

背景

警报素细胞因子白细胞介素-25（IL-25）在哮喘和伴鼻息肉的慢性鼻-鼻窦炎（CRSwNP）等疾病中促进2型炎症反应，已知靶点包括2型固有淋巴细胞（ILC2）和辅助性T细胞2（Th2细胞）。然而，IL-25的其他细胞靶点仍不清楚。

目的

研究B细胞对IL-25受体（IL-17RB）的诱导和表达，并评估体外表达IL-17RB的B细胞对IL-25的反应性。

方法

采用流式细胞术和逆转录-聚合酶链反应（RT-PCR）评估外周血来源的B细胞中IL-17RB的表达、调节及其在B细胞上的功能，包括对诱导IgE产生的刺激（抗CD40单克隆抗体和IL-4）的反应。使用单细胞RNA测序比较IL-17RB⁺和IL-17RB激活的外周血来源的B细胞。为了评估2型炎症组织中B细胞IL-17RB的表达，比较了鼻息肉、对照鼻甲组织和匹配外周血中的B细胞。

结果

用抗CD40和IL-4激活B细胞可增加蛋白和mRNA水平的IL-17RB表达，IL-25可进一步上调其表达。诱导表达IL-17RB的B细胞对IL-25反应，抗体产生增加。单细胞RNA测序显示，与IL-17RB⁻ B细胞相比，IL17RB⁺激活的B细胞表达更高水平的免疫球蛋白E（IGHE）、趋化因子（C-C基序）配体17（CCL17）和趋化因子（C-C基序）配体22（CCL22）。鼻息肉组织中的B细胞比对照组织表达更高水平的表面IL-17RB，这与患者报告的CRSwNP严重程度（鼻窦炎结局测试-22[SNOT-22]）相关。

结论

在诱导IgE产生的条件下激活的外周血B细胞表达表面IL-17RB，并且在2型炎症中组织IL-17RB⁺ B细胞增加。IL-17RB⁺细胞具有独特的转录谱，并对IL-25反应，抗体产生增加，突出了IL-25/IL-17RB途径作为CRSwNP和其他2型炎症性疾病的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/56cc0ba4022f/ALL-80-965-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/ff84b9ff2d06/ALL-80-965-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/b0dd4866f778/ALL-80-965-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/bad26d014b6f/ALL-80-965-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/a31fa4e5f0af/ALL-80-965-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/56cc0ba4022f/ALL-80-965-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/ff84b9ff2d06/ALL-80-965-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/b0dd4866f778/ALL-80-965-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/bad26d014b6f/ALL-80-965-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/a31fa4e5f0af/ALL-80-965-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/11969324/56cc0ba4022f/ALL-80-965-g006.jpg

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