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双特异性抗体连接先天受体诱导人类耐受树突状细胞和调节性 T 细胞。

Bispecific antibodies tethering innate receptors induce human tolerant-dendritic cells and regulatory T cells.

机构信息

EA7501, Groupe Innovation et Ciblage Cellulaire, Team Fc Récepteurs, Anticorps et MicroEnvironnement (FRAME), Université de Tours, Tours, France.

Infectiologie et Santé Publique (ISP) UMR 1282, INRAE, Team BioMAP, Université de Tours, Tours, France.

出版信息

Front Immunol. 2024 Mar 26;15:1369117. doi: 10.3389/fimmu.2024.1369117. eCollection 2024.

DOI:10.3389/fimmu.2024.1369117
PMID:38601165
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11005913/
Abstract

There is an urgent need for alternative therapies targeting human dendritic cells (DCs) that could reverse inflammatory syndromes in many autoimmune and inflammatory diseases and organ transplantations. Here, we describe a bispecific antibody (bsAb) strategy tethering two pathogen-recognition receptors at the surface of human DCs. This cross-linking switches DCs into a tolerant profile able to induce regulatory T-cell differentiation. The bsAbs, not parental Abs, induced interleukin 10 and transforming growth factor β1 secretion in monocyte-derived DCs and human peripheral blood mononuclear cells. In addition, they induced interleukin 10 secretion by synovial fluid cells in rheumatoid arthritis and gout patients. This concept of bsAb-induced tethering of surface pathogen-recognition receptors switching cell properties opens a new therapeutic avenue for controlling inflammation and restoring immune tolerance.

摘要

目前非常需要针对人类树突状细胞 (DC) 的替代疗法，这种疗法可能逆转许多自身免疫和炎症性疾病以及器官移植中的炎症综合征。在这里，我们描述了一种双特异性抗体 (bsAb) 策略，该策略将两种病原体识别受体在人类 DC 的表面连接在一起。这种交联将 DC 转换为具有耐受特征的细胞，能够诱导调节性 T 细胞分化。bsAbs（而不是亲本 Abs）在单核细胞衍生的 DC 和人外周血单核细胞中诱导白细胞介素 10 和转化生长因子 β1 的分泌。此外，它们还诱导类风湿关节炎和痛风患者的滑液细胞分泌白细胞介素 10。这种 bsAb 诱导的表面病原体识别受体交联从而改变细胞特性的概念为控制炎症和恢复免疫耐受开辟了新的治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/b9aa32dc23f7/fimmu-15-1369117-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/9e72a5de2e64/fimmu-15-1369117-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/a3f9ab1f0fc0/fimmu-15-1369117-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/67e3da46f3b9/fimmu-15-1369117-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/9b5c5b9593e0/fimmu-15-1369117-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/b9aa32dc23f7/fimmu-15-1369117-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/9e72a5de2e64/fimmu-15-1369117-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/a3f9ab1f0fc0/fimmu-15-1369117-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/67e3da46f3b9/fimmu-15-1369117-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/9b5c5b9593e0/fimmu-15-1369117-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4604/11005913/b9aa32dc23f7/fimmu-15-1369117-g005.jpg

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