Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Fine specificity of the myelin-reactive T cell repertoire: implications for TCR antagonism in autoimmunity.

Journal of immunology (Baltimore, Md. : 1950) - 1 Oct 1998

Anderton S M, Manickasingham S P, Burkhart C, Luckcuck T A, Holland S J, Lamont A G, Wraith D C

Abstract excerpt

The use of altered peptide ligands (APL) to modulate T cell responses has been suggested as a means of treating T cell-mediated autoimmune disorders. We have assessed the therapeutic potential of TCR antagonist peptides in autoimmunity using murine experimental autoimmune encephalomyelitis (EAE) as a model. The Tg4 transgenic mouse expresses an MHC class II-restricted TCR specific for the immunodominant...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amino Acid Sequence
Share to Cell Line

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Mice, Inbred C57BL

Share to Mice, Inbred Strains

Share to Mice, Transgenic

Share to Molecular Sequence Data

Share to Phenotype

Source

Identifiers

PMID: 9759852

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Fine specificity of the myelin-reactive T cell repertoire: implications for TCR antagonism in autoimmunity.PMID 9759852Read ↗

Amino acid variations at a single residue in an autoimmune peptide profoundly affect its properties: T-cell activation, major histocompatibility complex binding, and ability to block experimental allergic encephalomyelitis.Semantic proximity Read ↗

Negative Selection during the Peripheral Immune Response to AntigenSemantic proximity Read ↗

Targeted suppression of autoreactive CD8+ T-cell activation using blocking anti-CD8 antibodiesSemantic proximity Read ↗

Subtle affinity-enhancing mutations in a myelin oligodendrocyte glycoprotein-specific TCR alter specificity and generate new self-reactivity.Semantic proximity Read ↗

A single amino acid change in a myelin basic protein peptide confers the capacity to prevent rather than induce experimental autoimmune encephalomyelitis.Semantic proximity Read ↗

Retrogenic modeling of experimental allergic encephalomyelitis associates T cell frequency but not TCR functional affinity with pathogenicity.Semantic proximity Read ↗

CTLA-4 controls the thymic development of both conventional and regulatory T cells through modulation of the TCR repertoireSemantic proximity Read ↗

Incomplete TCR-β allelic exclusion accelerates spontaneous autoimmune arthritis in K/BxN TCR transgenic mice.Semantic proximity Read ↗

Interactions among polymorphic and conserved residues in MHC class II proteins affect MHC-peptide conformation and T cell recognition.Semantic proximity Read ↗

Autopathogenic T helper cell type 1 (Th1) and protective Th2 clones differ in their recognition of the autoantigenic peptide of myelin proteolipid protein.Semantic proximity Read ↗

T-cell receptors: germline polymorphism and patterns of usage in demyelinating diseases.Semantic proximity Read ↗

The T-cell response to myelin basic protein in familial multiple sclerosis: diversity of fine specificity, restricting elements, and T-cell receptor usage.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.