ArticleThe Journal of clinical investigation2001
Requirement for endocytic antigen processing and influence of invariant chain and H-2M deficiencies in CNS autoimmunity.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 89 citations in OpenAlex.
- Translational insights from EAE models : decoding MOGAD pathogenesis and therapeutic innovation.Frontiers in immunology · 2025Review
- MOG CNS Autoimmunity and MOGAD.Neurology(R) neuroimmunology & neuroinflammation · 2024Review
- TREX1 is required for microglial cholesterol homeostasis and oligodendrocyte terminal differentiation in human neural assembloids.Molecular psychiatry · 2024Article
- T cell deletional tolerance restricts AQP4 but not MOG CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function.Acta neuropathologica · 2022Review
- Pik3c3 deficiency in myeloid cells imparts partial resistance to experimental autoimmune encephalomyelitis associated with reduced IL-1β production.Cellular & molecular immunology · 2021Article
- CNS-resident classical DCs play a critical role in CNS autoimmune disease.The Journal of clinical investigation · 2018Article
- Tregs restrain dendritic cell autophagy to ameliorate autoimmunity.The Journal of clinical investigation · 2017Article
- Human leukocyte Antigen-DM polymorphisms in autoimmune diseases.Open biology · 2016Review
- Vitamin D3 Suppresses Class II Invariant Chain Peptide Expression on Activated B-Lymphocytes: A Plausible Mechanism for Downregulation of Acute Inflammatory Conditions.Journal of nutrition and metabolism · 2016Article
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- B cell antigen presentation is sufficient to drive neuroinflammation in an animal model of multiple sclerosis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Does MOG Ig-positive AQP4-seronegative opticospinal inflammatory disease justify a diagnosis of NMO spectrum disorder?Neurology(R) neuroimmunology & neuroinflammation · 2015Review
- Immune surveillance of the central nervous system in multiple sclerosis--relevance for therapy and experimental models.Journal of neuroimmunology · 2014Review
- Traumatic brain injury causes selective, CD74-dependent peripheral lymphocyte activation that exacerbates neurodegeneration.Acta neuropathologica communications · 2014Article
- Immunodominant T-cell epitopes of MOG reside in its transmembrane and cytoplasmic domains in EAE.Neurology(R) neuroimmunology & neuroinflammation · 2014Article
- Apolipoprotein E mediation of neuro-inflammation in a murine model of multiple sclerosis.Journal of neuroimmunology · 2014Article
- Virus-encoded ectopic CD74 enhances poxvirus vaccine efficacy.Immunology · 2014Article
- MHC class II-dependent B cell APC function is required for induction of CNS autoimmunity independent of myelin-specific antibodies.The Journal of experimental medicine · 2013Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The role of processing in antigen (Ag) presentation and T cell activation in experimental allergic encephalomyelitis (EAE) was evaluated in wild-type mice, mice that selectively express either Ii p31 or p41, and mice completely deficient in Ii or H-2M. We demonstrate that processing of myelin oligodendrocyte glycoprotein (MOG) is required for presentation of the dominant encephalitogenic MOG epitope, p35-55. Ii p31- and p41-expressing mice developed EAE with similar incidence to wild-type mice, although p41 mice had a more severe course. Ag-presenting cells (APCs) from Ii- or H-2M-deficient mice could present p35-55, but not MOG, demonstrating that these APCs could not process native MOG. Ii- and H-2M-deficient mice were not susceptible to EAE by immunization with p35-55 or MOG or by adoptive transfer of encephalitogenic T cells. However, CD4+ T cells from p35-55-immunized H-2M-deficient mice proliferated, secreted IFN-gamma, and transferred EAE to wild-type, but not H-2M-deficient, mice. Thus, EAE resistance in H-2M-deficient mice is not due to an inability of APCs to present p35-55, or an intrinsic defect in the encephalitogenic T cell repertoire, but reflects a defect in APC function. Our results indicate that processing is required for initial Ag presentation and CNS T cell activation and suggest that autopathogenic peptides of CNS autoantigen may not be readily available for presentation without processing.
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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.