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Updated: Feb 14, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
The Macrophage Mannose Receptor Regulate Mannan-Induced Psoriasis, Psoriatic Arthritis, and Rheumatoid Arthritis-Like
Cecilia Hagert1,2, Outi Sareila1,3, Tiina Kelkka1,4
1Medicity Research Laboratory, University of Turku, Turku, Finland.
Abstract:
The injection of mannan into mice can result in the development of psoriasis (Ps) and psoriatic arthritis (PsA), whereas co-injection with antibodies toward collagen type II leads to a chronic rheumatoid-like arthritis. The critical event in all these diseases is mannan-mediated activation of macrophages, causing more severe disease if the macrophages are deficient in neutrophil cytosolic factor 1 (Ncf1), i.e., lack the capacity to make a reactive oxygen species (ROS) burst. In this study, we investigated the role of one of the receptors binding mannan; the macrophage mannose receptor (MR, CD206). MR is a C-type lectin present on myeloid cells and lymphatics. We found that mice deficient in MR expression had more severe mannan-induced Ps, PsA as well as rheumatoid-like arthritis. Interestingly, the MR-mediated protection was partly lost in Ncf1 mutated mice and was associated with an type 2 macrophage expansion. In conclusion, these results show that MR protects against a pathogenic inflammatory macrophage response induced by mannan and is associated with induction of ROS.
Insights
Mannose receptor (MR) deficiency exacerbates mannan-induced inflammatory diseases like psoriasis and arthritis in mice. MR protects against severe disease by regulating macrophage responses and reactive oxygen species (ROS) production.
Area of Science:
- Immunology
- Inflammation Research
- Macrophage Biology
Background:
- Mannan injection in mice induces psoriasis (Ps) and psoriatic arthritis (PsA).
- Neutrophil cytosolic factor 1 (Ncf1) deficiency worsens these conditions by impairing reactive oxygen species (ROS) burst in macrophages.
- The macrophage mannose receptor (MR, CD206) binds mannan and is investigated for its role in these inflammatory diseases.
Purpose of the Study:
- To investigate the role of the macrophage mannose receptor (MR, CD206) in mannan-induced inflammatory conditions.
- To determine how MR deficiency affects the severity of psoriasis, psoriatic arthritis, and rheumatoid-like arthritis.
- To explore the interplay between MR, Ncf1, and macrophage activation in disease pathogenesis.
Main Methods:
- Utilized mouse models deficient in MR expression.
- Induced inflammatory conditions using mannan injection, with and without antibodies to collagen type II.
- Analyzed disease severity and characterized macrophage populations, including Ncf1 status and ROS production.
Main Results:
- Mice deficient in MR exhibited more severe mannan-induced Ps, PsA, and rheumatoid-like arthritis.
- MR-mediated protection was diminished in Ncf1-mutated mice.
- The protective effect of MR was associated with a type 2 macrophage expansion and ROS induction.
Conclusions:
- Macrophage mannose receptor (MR) plays a protective role against pathogenic inflammatory responses induced by mannan.
- MR signaling is crucial for regulating macrophage activation and ROS production in inflammatory arthritis and psoriasis.
- Targeting MR may offer therapeutic potential for inflammatory diseases driven by mannan-mediated pathways.
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