ArticleJournal of immunology (Baltimore, Md. : 1950)2014
HLA-DRα1 constructs block CD74 expression and MIF effects in experimental autoimmune encephalomyelitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
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- Neuronal and glial networks interact with traumatic brain injury to modulate cognition in ABCD study.NPJ systems biology and applications · 2026Article
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- MIF contribution to progressive brain diseases.Journal of neuroinflammation · 2024Review
- Macrophage migration inhibitory factor receptor CD74 expression is associated with expansion and differentiation of effector T cells in COVID-19 patients.Frontiers in immunology · 2023Article
- Novel therapeutic for multiple sclerosis protects white matter function in EAE mouse model.Frontiers in molecular medicine · 2023Article
- The development of endoplasmic reticulum-related gene signatures and the immune infiltration analysis of sepsis.Frontiers in immunology · 2023Article
- "Near Cure" treatment of severe acute EAE in MIF-1-deficient female and male mice with a bifunctional MHCII-derived molecular construct.Cellular immunology · 2022Article
- Brief report: Enhanced DRα1-mMOG-35-55 treatment of severe EAE in MIF-1-deficient male mice.Cellular immunology · 2021Article
- Review
- Spleen participation in partial MHC class II construct neuroprotection in stroke.CNS neuroscience & therapeutics · 2020Review
- MIF-Dependent Control of Tumor Immunity.Frontiers in immunology · 2020Review
- Macrophage migration inhibitory factor (MIF) as a therapeutic target for rheumatoid arthritis and systemic lupus erythematosus.Expert opinion on therapeutic targets · 2019Review
- Increased CD74 binding and EAE treatment efficacy of a modified DRα1 molecular construct.Metabolic brain disease · 2019Article
- A novel neurotherapeutic for multiple sclerosis, ischemic injury, methamphetamine addiction, and traumatic brain injury.Journal of neuroinflammation · 2019Review
- Blockade of MIF-CD74 Signalling on Macrophages and Dendritic Cells Restores the Antitumour Immune Response Against Metastatic Melanoma.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
CD74, the cell-surface form of the MHC class II invariant chain, is a key inflammatory factor that is involved in various immune-mediated diseases as part of the macrophage migration inhibitory factor (MIF) binding complex. However, little is known about the natural regulators of CD74 in this context. In order to study the role of the HLA-DR molecule in regulating CD74, we used the HLA-DRα1 domain, which was shown to bind to and downregulate CD74 on CD11b(+) monocytes. We found that DRα1 directly inhibited binding of MIF to CD74 and blocked its downstream inflammatory effects in the spinal cord of mice with experimental autoimmune encephalomyelitis (EAE). Potency of the DRα1 domain could be destroyed by trypsin digestion but enhanced by addition of a peptide extension (myelin oligodendrocyte glycoprotein [MOG]-35-55 peptide) that provided secondary structure not present in DRα1. These data suggest a conformationally sensitive determinant on DRα1-MOG that is responsible for optimal binding to CD74 and antagonism of MIF effects, resulting in reduced axonal damage and reversal of ongoing clinical and histological signs of EAE. These results demonstrate natural antagonist activity of DRα1 for MIF that was strongly potentiated by the MOG peptide extension, resulting in a novel therapeutic, DRα1-MOG-35-55, that within the limitations of the EAE model may have the potential to treat autoimmune diseases such as multiple sclerosis.
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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.