ArticleFrontiers in immunology2017
Epitope-Specific Tolerance Modes Differentially Specify Susceptibility to Proteolipid Protein-Induced Experimental Autoimmune Encephalomyelitis.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cathepsin L-dependent positive selection shapes clonal composition and functional fitness of CD4Nature immunology · 2025Article
- Secrets and lies of host-microbial interactions: MHC restriction and trans-regulation of T cell trafficking conceal the role of microbial agents on the edge between health and multifactorial/complex diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Active Induction of a Multiple Sclerosis-Like Disease in Common Laboratory Mouse Strains.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Isolated catatonia-like executive dysfunction in mice with forebrain-specific loss of myelin integrity.eLife · 2023Article
- The contribution of thymic tolerance to central nervous system autoimmunity.Seminars in immunopathology · 2021Review
- Breakdown of T-cell ignorance: The tolerance failure responsible for mainstream autoimmune diseases?Journal of translational autoimmunity · 2020Review
- Inventories of naive and tolerant mouse CD4 T cell repertoires reveal a hierarchy of deleted and diverted T cell receptors.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
9 authors.
Funding
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Abstract
Immunization with myelin components can elicit experimental autoimmune encephalomyelitis (EAE). EAE susceptibility varies between mouse strains, depending on the antigen employed. BL/6 mice are largely resistant to EAE induction with proteolipid protein (PLP), probably a reflection of antigen-specific tolerance. However, the extent and mechanism(s) of tolerance to PLP remain unclear. Here, we identified three PLP epitopes in PLP-deficient BL/6 mice. PLP-sufficient mice did not respond against two of these, whereas tolerance was "leaky" for an epitope with weak predicted MHCII binding, and only this epitope was encephalitogenic. In TCR transgenic mice, the "EAE-susceptibility-associated" epitope was "ignored" by specific CD4 T cells, whereas the "resistance-associated" epitope induced clonal deletion and T
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