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Titolo:
Molecular mimicry in type 1 diabetes mellitus revisited: T-cell clones to GAD65 peptides with sequence homology to coxsackie or proinsulin peptides do not crossreact with homologous counterpart
Autore:
Schloot, NC; Willemen, SJM; Duinkerken, G; Drijfhout, JW; de Vries, RRP; Roep, BO;
Indirizzi:
Leiden Univ, Med Ctr, Dept Immunohematol & Blood Transfus, NL-2333 ZA Leiden, Netherlands Leiden Univ Leiden Netherlands NL-2333 ZA NL-2333 ZA Leiden, Netherlands
Titolo Testata:
HUMAN IMMUNOLOGY
fascicolo: 4, volume: 62, anno: 2001,
pagine: 299 - 309
SICI:
0198-8859(200104)62:4<299:MMIT1D>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTAMIC-ACID DECARBOXYLASE; RECENT-ONSET IDDM; BLOOD MONONUCLEAR-CELLS; MYELIN BASIC-PROTEIN; NOD MICE; AUTOIMMUNE-DISEASE; TRANSGENIC MICE; ISLET ANTIGENS; INSULIN; VIRUS;
Keywords:
molecular mimicry; autoimmune disease; Coxsackie virus; GAD65; proinsulin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Roep, BO Leiden Univ, Med Ctr, Dept Immunohematol & Blood Transfus, Albinusdreef 2,NL-2333 ZA Leiden, Netherlands Leiden Univ Albinusdreef 2 Leiden Netherlands NL-2333 ZA erlands
Citazione:
N.C. Schloot et al., "Molecular mimicry in type 1 diabetes mellitus revisited: T-cell clones to GAD65 peptides with sequence homology to coxsackie or proinsulin peptides do not crossreact with homologous counterpart", HUMAN IMMUN, 62(4), 2001, pp. 299-309

Abstract

Type 1 diabetes mellitus is a T-cell mediated autoimmune disease in which the insulin-producing pancreatic beta cells are selectively destroyed. Molecular mimicry and T-cell crossreactivity to p-cell autoantigens and environmental agents with sequence similarities have been a proposed mechanism underlying the pathogenesis oi type 1 diabetes, but actual crossreactivity hasnot yet been demonstrated. We isolated and investigated T cells reactive to GAD65 peptides and homologous peptides of che Coxsackie virus protein P2Cand proinsulin from recent onset type 1 diabetes patients, and tested their fine specificity and cytokine production profile. Six T-cell lines specific for GAD65 peptides (amino acids 491-530) with homology to proinsulin (B20-C14) were isolated from six newly diagnosed patients with type 1 diabetes, but none of the stable T-cell lines crossreacted to the homologous proinsulin peptides. Similarly, none of four T-cell lines reactive to GAD65 peptides (amino acids 247-280) with sequence homology Io Coxsackie P2C (amino acids 30-50) crossreacted to the homologous viral peptide. Two T-cell lines corecognized a GAD65 peptide and a Coxsackie P2C peptide. However, the antigen-specific T-cell clones from these T-cell lines were reacting either withthe GAD65 peptide or the Coxsackie P2C peptide using different restrictionelements without crossreacting to the homologous peptide. Our data demon strate that homologous peptides previously proposed to serve as targets for crossreactivity indeed are immunogenic. Yet, T-cell clones did not crossreact with linear sequence homologies, despite strong T-cell responses to individual peptides. (C) American Society for Histocompatibility and Immunogenetics, 2001. Published by Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 00:53:00