ArticlePloS one2014
A potential role of myeloid DAP12-associating lectin (MDL)-1 in the regulation of inflammation in rheumatoid arthritis patients.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Review
- A Pan-Cancer Analysis Reveals CLEC5A as a Biomarker for Cancer Immunity and Prognosis.Frontiers in immunology · 2022Article
- Activation of the Innate Immune Checkpoint CLEC5A on Myeloid Cells in the Absence of Danger Signals Modulates Macrophages' Function but Does Not Trigger the Adaptive T Cell Immune Response.Journal of immunology research · 2022Article
- Genetic loss-of-function of activating transcription factor 3 but not C-type lectin member 5A prevents diabetic peripheral neuropathy.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Role of OSCAR Signaling in Osteoclastogenesis and Bone Disease.Frontiers in cell and developmental biology · 2021Review
- Elevated Expression of C-Type Lectin Domain Family 5-Member A (CLEC5A) and Its Relation to Inflammatory Parameters and Disease Course in Adult-Onset Still's Disease.Journal of immunology research · 2020Article
- CLEC5A: A Promiscuous Pattern Recognition Receptor to Microbes and Beyond.Advances in experimental medicine and biology · 2020Review
- C-type lectins in immunity and homeostasis.Nature reviews. Immunology · 2018Review
- The macrophage C-type lectin receptor CLEC5A (MDL-1) expression is associated with early plaque progression and promotes macrophage survival.Journal of translational medicine · 2017Article
- CLEC5A is critical for dengue virus-induced osteoclast activation and bone homeostasis.Journal of molecular medicine (Berlin, Germany) · 2016Article
- A Comprehensive Review of Immunoreceptor Regulation of Osteoclasts.Clinical reviews in allergy & immunology · 2016Review
- Osteoimmunology: Major and Costimulatory Pathway Expression Associated with Chronic Inflammatory Induced Bone Loss.Journal of immunology research · 2015Review
- Inactivation of DAP12 in PMN inhibits TREM1-mediated activation in rheumatoid arthritis.PloS one · 2015Article
- Changes of rabbit meniscus influenced by hyaline cartilage injury of osteoarthritis.International journal of clinical and experimental medicine · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenic roles of myeloid DAP12-associating lectin-1(MDL-1) and DAP12 in human rheumatoid arthritis (RA) remain unknown. Frequencies of MDL-1-expressing monocytes in 22 active RA patients, 16 inactive RA patients, 12 osteoarthritis (OA) patients and 10 healthy controls (HC) were determined by flow-cytometry analysis. The mRNA expression levels of MDL-1 and DAP12 on PBMCs were evaluated by quantitative PCR, and their protein expression levels in the synovium were examined by immunohistochemistry. Significantly higher median percentages of circulating MDL-1-expressing monocytes were observed in active RA patients (53.6%) compared to inactive RA patients (34.1%), OA patients (27.9%), and HC (21.2%). Levels of MDL-1 and DAP12 gene expression in PBMCs and their protein expression in the synovium were significantly higher in active RA patients than in inactive RA or OA patients. MDL-1 levels were positively correlated with parameters of disease activity, articular damage, and levels of proinflammatory cytokines. MDL-1 activator (Dengue virus type 2 antigen) stimulation on PBMCs resulted in significantly enhanced levels of proinflammatory cytokines in RA patients compared to those in OA patients or HC, indicating that MDL-1 activation is functional. Frequencies of MDL-1-expressing monocytes and levels of MDL-1 and DAP12 gene expression significantly decreased after effective therapy. Concordant overexpression of MDL-1 and DAP12 were correlated with increased production of proinflammatory cytokines in RA patients, suggesting their roles in regulating articular inflammation.
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