A Self-Developed IL-6Rα Nanobody Alleviates Experimental Autoimmune Uveitis by Inhibiting Th1 and Th17 Cells
4 affiliations
- 1Department of Ophthalmology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001 P.R. China
- 2Department of Medical Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001 China
- 3Bengbu Medical University, Bengbu, Anhui China
- 4Department of Ophthalmology, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001 China
Abstract
Interleukin-6, a pleiotropic cytokine, initiates downstream signaling by binding to interleukin-6 receptor α (IL-6Rα) and glycoprotein 130 (GP130). Autoimmune uveitis, the most prevalent form of non-infectious uveitis, represents a serious sight-threatening ocular disorder. While corticosteroids remain the mainstay of treatment in clinical practice, their therapeutic utility is constrained by significant adverse effects. Emerging evidence highlights the pivotal role of IL-6 in autoimmune uveitis pathogenesis, particularly in promoting CD4+T cells differentiation into Type 17 helper T cells (Th17). In this study, we evaluated the therapeutic efficacy of a novel anti-IL-6Rα nanobody in experimental autoimmune uveitis (EAU) models. Peripheral blood mononuclear cells (PBMCs) from Vogt-Koyanagi-Harada (VKH) patients were used to further assess the translational relevance of the anti-IL-6Rα nanobody. Our results demonstrate that this nanobody not only suppressed Type 17 helper T cells but also Type 1 helper T cells (Th1). Furthermore, treatment with anti-IL-6Rα nanobody significantly reduced inflammatory mediators and ameliorated disease severity in murine models. In vitro studies using PBMCs from VKH patients revealed that the anti-IL-6Rα nanobody effectively suppressed both interferon-γ (IFN-γ) and IL-17 production. These findings collectively suggest that anti-IL-6Rα nanobody represents a promising therapeutic strategy for autoimmune uveitis.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s10753-026-02540-4.
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BibTeX
@article{yao2026selfdeveloped,
title = {{A Self-Developed IL-6Rα Nanobody Alleviates Experimental Autoimmune Uveitis by Inhibiting Th1 and Th17 Cells}},
author = {Bochen Yao and Dali Tong and Jiaojiao Qian and Yuewei Peng and Zhouhuan Xi and Niannian Fan and Feiyu Jin and Can Deng and Bofeng Li and Kai Dong},
journal = {Inflammation},
year = {2026},
month = jul,
doi = {10.1007/s10753-026-02540-4},
url = {https://doi.org/10.1007/s10753-026-02540-4},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - A Self-Developed IL-6Rα Nanobody Alleviates Experimental Autoimmune Uveitis by Inhibiting Th1 and Th17 Cells
AU - Bochen Yao
AU - Dali Tong
AU - Jiaojiao Qian
AU - Yuewei Peng
AU - Zhouhuan Xi
AU - Niannian Fan
AU - Feiyu Jin
AU - Can Deng
AU - Bofeng Li
AU - Kai Dong
PY - 2026
DA - 2026/07/07
JO - Inflammation
DO - 10.1007/s10753-026-02540-4
UR - https://doi.org/10.1007/s10753-026-02540-4
AB - Interleukin-6, a pleiotropic cytokine, initiates downstream signaling by binding to interleukin-6 receptor α (IL-6Rα) and glycoprotein 130 (GP130). Autoimmune uveitis, the most prevalent form of non-infectious uveitis, represents a serious sight-threatening ocular disorder. While corticosteroids remain the mainstay of treatment in clinical practice, their therapeutic utility is constrained by significant adverse effects. Emerging evidence highlights the pivotal role of IL-6 in autoimmune uveitis pathogenesis, particularly in promoting CD4+T cells differentiation into Type 17 helper T cells (Th17). In this study, we evaluated the therapeutic efficacy of a novel anti-IL-6Rα nanobody in experimental autoimmune uveitis (EAU) models. Peripheral blood mononuclear cells (PBMCs) from Vogt-Koyanagi-Harada (VKH) patients were used to further assess the translational relevance of the anti-IL-6Rα nanobody. Our results demonstrate that this nanobody not only suppressed Type 17 helper T cells but also Type 1 helper T cells (Th1). Furthermore, treatment with anti-IL-6Rα nanobody significantly reduced inflammatory mediators and ameliorated disease severity in murine models. In vitro studies using PBMCs from VKH patients revealed that the anti-IL-6Rα nanobody effectively suppressed both interferon-γ (IFN-γ) and IL-17 production. These findings collectively suggest that anti-IL-6Rα nanobody represents a promising therapeutic strategy for autoimmune uveitis. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s10753-026-02540-4.
SN - 0360-3997
SN - 1573-2576
ER -