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CD169 is a marker for highly pathogenic phagocytes in multiple sclerosis
Jeroen Fj Bogie1, Ellen Boelen1, Els Louagie2
1Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium/School of Life Sciences, Transnationale Universiteit Limburg, Diepenbeek, Belgium.
Background:
Phagocytes, such as macrophages and microglia, are key effector cells in the pathophysiology of multiple sclerosis (MS). It is widely accepted that they instigate and promote neuroinflammatory and neurodegenerative events in MS. An increasing amount of studies indicate that Siglec-1, also known CD169, is a marker for activated phagocytes in inflammatory disorders.
Objective:
In this study, we set out to define how CD169+ phagocytes contribute to neuroinflammation in MS.
Methods:
CD169-diphtheria toxin receptor (DTR) mice, which express human DTR under control of the CD169 promoter, were used to define the impact of CD169+ cells on neuroinflammation. Flow cytometry and immunohistochemistry were utilized to determine the expression and distribution of CD169.
Results:
We show that CD169 is highly expressed by lesional and circulating phagocytes in MS and experimental autoimmune encephalomyelitis (EAE). Our data further indicate that CD169 represents a selective marker for early activated microglia in MS and EAE lesions. Depletion of CD169+ cells markedly reduced neuroinflammation and ameliorated disease symptoms in EAE-affected mice.
Conclusion:
Our findings indicate that CD169+ cells promote neuroinflammation. Furthermore, they suggest that CD169+ phagocytes play a key role in the pathophysiology of MS. Hence, targeting CD169+ phagocytes may hold therapeutic value for MS.
Insights
CD169+ phagocytes drive neuroinflammation in multiple sclerosis (MS). Targeting these activated phagocytes reduced disease severity in mouse models, suggesting a potential therapeutic strategy for MS.
Area of Science:
- Neuroimmunology
- Cellular and Molecular Medicine
Background:
- Phagocytes, including macrophages and microglia, are central to multiple sclerosis (MS) pathophysiology, driving neuroinflammation and neurodegeneration.
- Siglec-1 (CD169) is increasingly recognized as a marker for activated phagocytes in inflammatory conditions.
Purpose of the Study:
- To investigate the specific role of CD169-expressing phagocytes in MS-related neuroinflammation.
- To determine if CD169 can serve as a therapeutic target for MS.
Main Methods:
- Utilized CD169-diphtheria toxin receptor (DTR) mice for targeted depletion of CD169+ cells.
- Employed flow cytometry and immunohistochemistry to analyze CD169 expression and distribution in MS and EAE models.
Main Results:
- CD169 was highly expressed on lesional and circulating phagocytes in MS and experimental autoimmune encephalomyelitis (EAE).
- CD169 identified early-activated microglia in MS and EAE lesions.
- Depletion of CD169+ cells significantly reduced neuroinflammation and improved disease symptoms in EAE mice.
Conclusions:
- CD169+ cells are key drivers of neuroinflammation in MS.
- CD169+ phagocytes play a critical role in the disease's pathology.
- Targeting CD169+ phagocytes presents a promising therapeutic avenue for MS treatment.
