ArticleClinical and experimental immunology2020
MOSPD2 is a therapeutic target for the treatment of CNS inflammation.
Article in Clinical and experimental immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- LEAP2 triggers retromer-mediated membrane trafficking of MOSPD2 to promote chemotaxis in teleost monocytes/macrophages.Zoological research · 2025Article
- MOSPD2 regulates the activation state of αLβ2 integrin to control monocyte migration: applicability for treatment of chronic inflammatory diseases.Immunologic research · 2025Article
- Deciphering MOSPD1's impact on breast cancer progression and therapeutic response.Biology direct · 2024Article
- Identification of shared gene signatures and pathways for diagnosing osteoporosis with sarcopenia through integrated bioinformatics analysis and machine learning.BMC musculoskeletal disorders · 2024Article
- Article
- Involvement of POMC neurons in LEAP2 regulation of food intake and body weight.Frontiers in endocrinology · 2022Article
- Article
- Clinical & Experimental Immunology: Highlights of 2020.Clinical and experimental immunology · 2021Article
- MOSPD2 is a receptor mediating the LEAP-2 effect on monocytes/macrophages in a teleost,Zoological research · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), myeloid cells comprise a major part of the inflammatory infiltrate in the central nervous system (CNS). We previously described that motile sperm domain-containing protein 2 (MOSPD2) is expressed on human myeloid cells and regulates monocyte migration in vitro. The role of MOSPD2 in EAE pathogenesis was studied by generating MOSPD2 knock-out (KO) mice and monoclonal antibodies directed against MOSPD2. We found that EAE development in MOSPD2 KO mice was significantly suppressed. While frequency representation of leukocyte subsets in lymphoid tissues was comparable, the ratio of inflammatory monocytes in the blood was markedly reduced in MOSPD2 KO mice. In addition, T cells from MOSPD2 KO mice displayed reduced secretion of proinflammatory cytokines and increased production of interleukin (IL)-4. Prophylactic and post-onset treatment using monoclonal antibodies (mAbs) generated against MOSPD2 abrogated development and reduced EAE severity. These results suggest that MOSPD2 is key in regulating migration of inflammatory monocytes, and that anti-MOSPD2 mAbs constitute a potential therapy for the treatment of CNS inflammatory diseases.
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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.