The mechanisms of hydroxychloroquine in rheumatoid arthritis treatment: inhibition of dendritic cell functions via Toll like receptor 9 signaling
Open accessAbstract
Hydroxychloroquine (HCQ) is one of the most commonly prescribed immune-suppressants in treating rheumatoid arthritis (RA). Our previous research showed that HCQ suppressed RA development by inhibiting T follicular helper (Tfh) cells directly. Dendritic cells (DCs) serve as the link between innate and acquired immunity. Whether HCQ suppressed Tfh cell through DCs was not clear. In current study, we found that HCQ efficiently inhibited CD86, chemokine (C-X-C motif) receptor 4 (CXCR4) expression and interferon-α (IFN-α) secretion of healthy donor derived purified DCs stimulated by RA patient serum. To mimic RA, collagen-induced arthritis (CIA) mouse model was used and treated with HCQ daily for fifty-four days prior to sacrifice. We found HCQ inhibited DC maturation and migration to lymph nodes (LNs), manifested as down-regulated expression of CD40, CD80, CD86, MHCII (I-Aq) on LN DCs. In addition, HCQ reduced the level of chemokine receptor 7 (CCR7) and L-selectin on peripheral blood DCs and diminished percentage of LN DCs. Of note, HCQ only inhibited CpG ODN 1826-induced IL-12 secretion by bone marrow DCs (BMDCs) stimulated by various toll like receptor (TLR) agonists. Mechanistically, HCQ down-regulated the expression of TLR9 not only in healthy donor PBMC-derived DCs stimulated by RA patient serum, but also in LN DCs of CIA mice and CpG-activated BMDCs. Furthermore, arthritis scores in TLR9−/− mice were much lower than that in wild type mice with impaired maturity and migration capability of DCs. Collectively, activation of DCs contributes to the pathogenesis of RA and HCQ shows protective effects on RA by inhibition of DC activation via blocking TLR9.
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Hydroxychloroquine has been purported to interact with and antagonise the key intracellular nucleic acid sensors TLR9 and cGAS, which likely contribute to its clinical efficacy in rheumatoid arthritis and systemic lupus erythematosus.
“Hydroxychloroquine has been purported to interact with and antagonise the key intracellular nucleic acid sensors, TLR9 and cGAS, which likely contribute to its clinical efficacy in rheumatoid arthritis and systemic lupus erythematous (Han et al., 2020).”
From Gene Therapy-Associated Uveitis (GTAU): Understanding and mitigating the adverse immune response in retinal gene therapy (2025) · cites this paper as Han et al., 2020
The Discussion supports hydroxychloroquine blocking TLR9 in rheumatoid arthritis, but explicitly says it 'could only' block TLR9 and proposes combining it with a separate cGAS inhibitor. That contradicts the claim that this paper attributes cGAS antagonism to hydroxychloroquine. The cited passages do not establish this mechanism as contributing to its clinical efficacy in systemic lupus erythematosus; page numbers are unavailable in our copy. (LLM, conf=0.88)
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Autoimmune diseases and the role of Toll-like receptor-7 and -9 signaling cascades
Keller, E. J., Patel, N. B., & Jørgensen, T. N. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822564-6.00004-5
Hydroxychloroquine: Chemistry and Medicinal Applications
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Mesenchymal stem cells for rheumatoid arthritis
Ichim, T. E., Ramos, R. A., Agamirov, A., Berry, S. K., Rath, A. V., Bykoriz, V., Nicole, E. U., Vyrlanovitch, M., Azimi, N. A., Reynolds, S., et al. (2025) · Journal of Stem Cell Research & Therapeutics · doi:10.15406/jsrt.2025.10.00187
Mainieri, L., Kaufmann, A., Bucci, L., Grieshaber‐Bouyer, R., Bauer, S., & Solis, F. V. (2025) · Lara D. Veeken · doi:10.1093/rheumatology/keaf537
- Authors
- Han, J., Li, X., Luo, X., He, J., Huang, X., Zhou, Q., Han, Y., Jie, H., Zhuang, J., Li, Y., Yang, F., Zhai, Z., Wu, S., He, Y., Yang, B., & Sun, E.
- Affiliations
- Third Affiliated Hospital of Southern Medical University (CN)
- Peking University Shenzhen Hospital (CN)
- Guangdong Provincial People's Hospital (CN)
- Southern Medical University (CN)
- South China Normal University (CN)
- Corresponding author
- He, Yi
- Yang, Bin
- Sun, Erwei
- ORCID
- Venue
- Biomedicine & Pharmacotherapy
- Publisher
- Elsevier BV
- Published
- 2020-12
- Volume
- 132
- Pages
- 110848
- ISSN
- 0753-3322 (ISSN-L)
- PMC
- PMC7547638
- OpenAlex
- W3092456362
- Cited by
- 49
- References
- 46
- Citations by year
- 2026: 1 · 2025: 9 · 2024: 12 · 2023: 11 · 2022: 7 · 2021: 9
- FWCI
- 5.09
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Biomedicine & Pharmacotherapy (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- hydroxychloroquine, rheumatoid arthritis, dendritic cells, TLR9, T follicular helper cells, dendritic cell maturation, dendritic cell migration, interferon-alpha, CXCR4, CCR7, L-selectin, IL-12, collagen-induced arthritis, TLR9-deficient mice, immunosuppression
- MeSH terms
- Adult, Aged, Animals, Arthritis, Experimental, Arthritis, Rheumatoid, Dendritic Cells, Female, Humans, Hydroxychloroquine, Male, Mice, Inbred C57BL, Mice, Inbred DBA, Middle Aged, Signal Transduction, Down-Regulation, Case-Control Studies, Mice, Knockout, Antirheumatic Agents, Toll-Like Receptor 9, Mice
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