Research output per year
Research output per year
Jeroen F. J. Bogie, Jo Mailleux, Elien Wouters, Winde Jorissen, Elien Grajchen, Jasmine Vanmol, Kristiaan Wouters, Niels Hellings, Jack Van Horsen, Tim Vanmierlo, Jerome J. A. Hendriks*
Research output: Contribution to journal › Article › Academic › peer-review
Myelin-containing macrophages and microglia are the most abundant immune cells in active multiple sclerosis (MS) lesions. Our recent transcriptomic analysis demonstrated that collectin placenta 1 (CL-P1) is one of the most potently induced genes in macrophages after uptake of myelin. CL-P1 is a type II transmembrane protein with both a collagen-like and carbohydrate recognition domain, which plays a key role in host defense. In this study we sought to determine the dynamics of CL-P1 expression on myelin-containing phagocytes and define the role that it plays in MS lesion development. We show that myelin uptake increases the cell surface expression of CL-P1 by mouse and human macrophages, but not by primary mouse microglia in vitro. In active demyelinating MS lesions, CL-P1 immunoreactivity was localized to perivascular and parenchymal myelin-laden phagocytes. Finally, we demonstrate that CL-P1 is involved in myelin internalization as knockdown of CL-P1 markedly reduced myelin uptake. Collectively, our data indicate that CL-P1 is a novel receptor involved in myelin uptake by phagocytes and likely plays a role in MS lesion development.
Original language | English |
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Article number | 44794 |
Number of pages | 9 |
Journal | Scientific Reports |
Volume | 7 |
DOIs | |
Publication status | Published - 20 Mar 2017 |
Research output: Contribution to journal › Erratum / corrigendum / retractions › Academic