ArticleJournal of leukocyte biology2013
TLR2 deletion promotes arthritis through reduction of IL-10.
Article in Journal of leukocyte biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The trial behind it
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Intestinal Ischemia/Reperfusion Injury: Mechanisms, Diagnosis, and Therapeutic Advances.International journal of biological sciences · 2026Review
- Comprehensive analysis of myeloid reporter mice.bioRxiv : the preprint server for biology · 2025Article
- AHCC inhibited hepatic stellate cells activation by regulation of cytoglobin induction via TLR2-SAPK/JNK pathway and collagen production via TLR4-NF-κβ pathway.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Article
- Toll-like Receptor 2 in Autoimmune Inflammation.Immune network · 2021Review
- Transcriptional Profiling of Synovial Macrophages Using Minimally Invasive Ultrasound-Guided Synovial Biopsies in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2018Article
- Deletion of calponin 2 in macrophages attenuates the severity of inflammatory arthritis in mice.American journal of physiology. Cell physiology · 2016Article
- CD11c-mediated deletion of Flip promotes autoreactivity and inflammatory arthritis.Nature communications · 2015Article
- Pristimerin, a naturally occurring triterpenoid, protects against autoimmune arthritis by modulating the cellular and soluble immune mediators of inflammation and tissue damage.Clinical immunology (Orlando, Fla.) · 2014Article
- Inhibition of fucosylation reshapes inflammatory macrophages and suppresses type II collagen-induced arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Apolipoprotein a-I at the interface of vascular inflammation and arthritis.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- Toll-like receptor-mediated IRE1α activation as a therapeutic target for inflammatory arthritis.The EMBO journal · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
RA is a chronic inflammatory disease characterized by the persistent expression of inflammatory cytokines from macrophages, which may be mediated, in part, through TLR2 signaling. Earlier studies demonstrate a role for TLR2 signaling in dampening the arthritis in IL-1Ra-/- mice, which was mediated through T cells. This study was performed to determine whether TLR2 signaling plays a role in the pathogenesis of T cell-independent arthritis triggered by transferring serum from K/BxN mice. We documented more severe arthritis in Tlr2-/- mice compared with WT controls. The Tlr2-/- mice also demonstrated increased inflammation, erosion, pannus formation, and osteoclastogenesis, as well as increased IL-1β and decreased IL-10 within the joints. In vitro bone marrow-differentiated macrophages expressed comparable levels of activating and inhibitory FcγRs, however when stimulated with immune complexes, the Tlr2-/- macrophages expressed decreased IL-10 and reduced activation of Akt and ERK. Our findings indicate that Tlr2-/- promotes the effector phase of arthritis through decreased IL-10 by macrophages, which is important, not only as an anti-inflammatory cytokine but also in restraining the differentiation and activation of osteoclasts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.