Prevention of experimental autoimmune arthritis with a peptide fragment of type II collagen

Collagen arthritis is induced in inbred rats with the injection of native type II collagen. The pathogenesis of this experimental autoimmune disease is T cell dependent. This study demonstrates that collagen‐specific Tcells, derived from pathogenic and nonpathogenic rat Tcell lines, both recognize t...

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Veröffentlicht in:European journal of immunology 1993-03, Vol.23 (3), p.591-599
Hauptverfasser: Ku, Grace, Kronenberg, Mitchell, Peacock, Derek J., Tempst, Paul, Banquerigo, Mona Lisa, Braun, Benjamin S., Reeve, Joseph R., Brahn, Ernest
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container_end_page 599
container_issue 3
container_start_page 591
container_title European journal of immunology
container_volume 23
creator Ku, Grace
Kronenberg, Mitchell
Peacock, Derek J.
Tempst, Paul
Banquerigo, Mona Lisa
Braun, Benjamin S.
Reeve, Joseph R.
Brahn, Ernest
description Collagen arthritis is induced in inbred rats with the injection of native type II collagen. The pathogenesis of this experimental autoimmune disease is T cell dependent. This study demonstrates that collagen‐specific Tcells, derived from pathogenic and nonpathogenic rat Tcell lines, both recognize the same peptide epitope. The epitope, consisting of amino acids 58–73 of cyanogen bromide fragment 11 of type II collagen, was as effective as whole collagen in stimulating a panel of collagen‐specific rat/mouse Tcell hybridomas. This peptide may, therefore, constitute a dominant epitope for CD4+ rat Tcells in their response to type II collagen. Administration of the peptide to either neonatal or adult rats prevented the subsequent induction of experimental arthritis with whole collagen, demonstrating that the in vivo response to this dominant epitope is, therefore, relevant in the pathogenesis of arthritis. Despite its ability to prevent collagen‐induced arthritis, administration of this peptide in incomplete Freund's adjuvant intradermally did not induce disease.
doi_str_mv 10.1002/eji.1830230302
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The pathogenesis of this experimental autoimmune disease is T cell dependent. This study demonstrates that collagen‐specific Tcells, derived from pathogenic and nonpathogenic rat Tcell lines, both recognize the same peptide epitope. The epitope, consisting of amino acids 58–73 of cyanogen bromide fragment 11 of type II collagen, was as effective as whole collagen in stimulating a panel of collagen‐specific rat/mouse Tcell hybridomas. This peptide may, therefore, constitute a dominant epitope for CD4+ rat Tcells in their response to type II collagen. Administration of the peptide to either neonatal or adult rats prevented the subsequent induction of experimental arthritis with whole collagen, demonstrating that the in vivo response to this dominant epitope is, therefore, relevant in the pathogenesis of arthritis. 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The pathogenesis of this experimental autoimmune disease is T cell dependent. This study demonstrates that collagen‐specific Tcells, derived from pathogenic and nonpathogenic rat Tcell lines, both recognize the same peptide epitope. The epitope, consisting of amino acids 58–73 of cyanogen bromide fragment 11 of type II collagen, was as effective as whole collagen in stimulating a panel of collagen‐specific rat/mouse Tcell hybridomas. This peptide may, therefore, constitute a dominant epitope for CD4+ rat Tcells in their response to type II collagen. Administration of the peptide to either neonatal or adult rats prevented the subsequent induction of experimental arthritis with whole collagen, demonstrating that the in vivo response to this dominant epitope is, therefore, relevant in the pathogenesis of arthritis. 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The pathogenesis of this experimental autoimmune disease is T cell dependent. This study demonstrates that collagen‐specific Tcells, derived from pathogenic and nonpathogenic rat Tcell lines, both recognize the same peptide epitope. The epitope, consisting of amino acids 58–73 of cyanogen bromide fragment 11 of type II collagen, was as effective as whole collagen in stimulating a panel of collagen‐specific rat/mouse Tcell hybridomas. This peptide may, therefore, constitute a dominant epitope for CD4+ rat Tcells in their response to type II collagen. Administration of the peptide to either neonatal or adult rats prevented the subsequent induction of experimental arthritis with whole collagen, demonstrating that the in vivo response to this dominant epitope is, therefore, relevant in the pathogenesis of arthritis. 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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Amino Acid Sequence
Animal model
Animals
Antibodies - immunology
Arthritis, Experimental - prevention & control
Biological and medical sciences
Collagen - immunology
Collagen arthritis
Diseases of the osteoarticular system
Epitopes
Hypersensitivity, Delayed - immunology
Immune Tolerance
Immunization
Inflammatory joint diseases
Medical sciences
Molecular Sequence Data
Peptide therapy
Peptides - chemistry
Peptides - immunology
Rats
Rats, Inbred Strains
T cell epitope
T-Lymphocytes - immunology
Tolerance
title Prevention of experimental autoimmune arthritis with a peptide fragment of type II collagen
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