ArticleThe American journal of pathology2007
p150/95 (CD11c/CD18) expression is required for the development of experimental autoimmune encephalomyelitis.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- CD11c+ CD8 T cells cause IFN-γ-dependent autoimmune neuroinflammation that is restrained by PD-1 signaling.JCI insight · 2026Article
- Contribution of microglia/macrophage to the pathogenesis of TMEV infection in the central nervous system.Frontiers in microbiology · 2024Review
- Article
- Optical coherence tomography monitoring and diagnosing retinal changes in multiple sclerosis.Brain and behavior · 2021Review
- γδ T Cells Participating in Nervous Systems: A Story of Jekyll and Hyde.Frontiers in immunology · 2021Review
- Complement-dependent synapse loss and microgliosis in a mouse model of multiple sclerosis.Brain, behavior, and immunity · 2020Article
- Epigenetic activation of O-linked β-N-acetylglucosamine transferase overrides the differentiation blockage in acute leukemia.EBioMedicine · 2020Article
- Complement Receptors in Myeloid Cell Adhesion and Phagocytosis.Microbiology spectrum · 2016Review
- IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier.Molecular neurodegeneration · 2016Article
- Expression of CD11c Is Associated with Unconventional Activated T Cell Subsets with High Migratory Potential.PloS one · 2016Article
- Animal models of Multiple Sclerosis.European journal of pharmacology · 2015Review
- Leukocyte integrins: role in leukocyte recruitment and as therapeutic targets in inflammatory disease.Pharmacology & therapeutics · 2015Review
- Using EAE to better understand principles of immune function and autoimmune pathology.Journal of autoimmunity · 2013Review
- Targeted inhibition of complement using complement receptor 2-conjugated inhibitors attenuates EAE.Neuroscience letters · 2012Article
- Gut mucosal injury in neonates is marked by macrophage infiltration in contrast to pleomorphic infiltrates in adult: evidence from an animal model.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- CD11c controls herpes simplex virus 1 responses to limit virus replication during primary infection.Journal of virology · 2011Article
- Prevention of experimental cerebral malaria by Flt3 ligand during infection with Plasmodium berghei ANKA.Infection and immunity · 2011Article
- Absence of β2 integrins impairs regulatory T cells and exacerbates CD4+ T cell-dependent autoimmune carditis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Macrophages counteract demyelination in a mouse model of globoid cell leukodystrophy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Alpha4beta1 integrin mediates the recruitment of immature dendritic cells across the blood-brain barrier during experimental autoimmune encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
p150/95 (CD11c/CD18, CR4) is a member of the beta(2)-integrin family of adhesion molecules and is considered an important phagocytic receptor. The role of p150/95 in the development of central nervous system demyelinating diseases, including multiple sclerosis, remains unexplored. To determine p150/95-mediated mechanisms in experimental autoimmune encephalomyelitis (EAE), we performed EAE using CD11c-deficient (CD11c(-/-)) mice. EAE in CD11c(-/-) mice was significantly attenuated and characterized by markedly reduced spinal cord T-cell infiltration and interferon-gamma production by these cells. Adoptive transfer of antigen-restimulated T cells from wild-type to CD11c(-/-) mice produced significantly attenuated EAE, whereas transfer of CD11c(-/-) antigen-restimulated T cells to control mice induced a very mild, monophasic EAE. T cells from MOG(35-55) peptide-primed CD11c(-/-) mice displayed an unusual cytokine phenotype with elevated levels of interleukin (IL)-2, IL-4, and IL-12 but reduced levels of interferon-gamma, tumor necrosis factor-alpha, IL-10, IL-17, and transforming growth factor-beta compared with control mice. Overall, CD11c(-/-) T cells from primed mice proliferated comparably to that of control T cells on MOG(35-55) restimulation. Our results indicate that expression of p150/95 is critical on both T cells as well as other leukocytes for the development of demyelinating disease and may represent a novel therapeutic target for multiple sclerosis.
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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.