ArticleArthritis research & therapy2023
Tau deficiency inhibits classically activated macrophage polarization and protects against collagen-induced arthritis in mice.
Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Inflammation-driven bone erosion and reactive remodeling in experimental arthritis revealed by cortical bone surface analysis.Arthritis research & therapy · 2026Article
- Meningeal macrophages alleviate social memory defects in an early Alzheimer's disease model.Molecular psychiatry · 2026Article
- Tau is a receptor with low affinity for glucocorticoids and is required for glucocorticoid-induced bone loss.Cell research · 2025Article
- Increased tau-induced inflammatory responses are associated with a greater degree of atherosclerosis in progressive supranuclear palsy.Frontiers in aging neuroscience · 2025Article
- Crosstalk between bone and brain in Alzheimer's disease: Mechanisms, applications, and perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- The relationship of ALPK1, hyaluronic acid and M1 macrophage polarization in the temporomandibular joint synovitis.Journal of cellular and molecular medicine · 2024Article
- Molecular Mechanisms Linking Osteoarthritis and Alzheimer's Disease: Shared Pathways, Mechanisms and Breakthrough Prospects.International journal of molecular sciences · 2024Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundTau protein serves a pro-inflammatory function in neuroinflammation. However, the role of tau in other inflammatory disorders such as rheumatoid arthritis (RA) is less explored. This study is to investigate the role of endogenous tau and the potential mechanisms in the pathogenesis of inflammatory arthritis.
methodsWe established collagen-induced arthritis (CIA) model in wild-type and Tau-/- mice to compare the clinical score and arthritis incidence. Micro-CT analysis was used to evaluate bone erosion of ankle joints. Histological analysis was performed to assess inflammatory cell infiltration, cartilage damage, and osteoclast activity in the ankle joints. Serum levels of pro-inflammatory cytokines were measured by ELISA. The expression levels of macrophage markers were determined by immunohistochemistry staining and quantitative real-time PCR.
resultsTau expression was upregulated in joints under inflammatory condition. Tau deletion in mice exhibited milder inflammation and protected against the progression of CIA, evidenced by reduced serum levels of pro-inflammatory cytokines and attenuated bone loss, inflammatory cell infiltration, cartilage damage, and osteoclast activity in the ankle joints. Furthermore, tau deficiency led to the inhibition of classically activated type 1 (M1) macrophage polarization in the synovium.
conclusionTau is a previously unrecognized critical regulator in the pathogenesis of RA and may provide a potential therapeutic target for autoimmune and inflammatory joint diseases.
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