Induction of tolerance against the arthritogenic antigen with type-II collagen peptide-linked soluble MHC class II molecules

Yoon Kyung Park, Sundo Jung, Se-Ho Park

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

In murine collagen-induced arthritis (CIA), self-reactive T cells can recognize peptide antigens derived from type-II collagen (CII). Activation of T cells is an important mediator of autoimmune diseases. Thus, T cells have become a focal point of study to treat autoimmune diseases. In this study, we evaluated the efficacy of recombinant MHC class II molecules in the regulation of antigen-specific T cells by using a self peptide derived from CII (CII260-274; IAGFKGEQGPKGEPG) linked to mouse I-Aq in a murine CIA model. We found that recombinant I-Aq/CII260-274 molecules could be recognized by CII-specific T cells and inhibit the same T cells in vitro. Furthermore, the development of CIA in mice was successfully prevented by in vivo injection of recombinant I-Aq/CII260-274 molecules. Thus, treatment with recombinant soluble MHC class II molecules in complex with an immunodominant self-peptide might offer a potential therapeutic for chronic inflammation in autoimmune disease such as rheumatoid arthritis.

Original languageEnglish
Pages (from-to)331-336
Number of pages6
JournalBMB Reports
Volume49
Issue number6
DOIs
Publication statusPublished - 2016

Fingerprint

T-cells
Collagen Type II
T-Lymphocytes
Antigens
Peptides
Molecules
Experimental Arthritis
Autoimmune Diseases
Collagen
Rheumatoid Arthritis
Chemical activation
Inflammation
Injections
Therapeutics

Keywords

  • Collagen-induced arthritis
  • Immunotherapy
  • Recombinant MHC II
  • Rheumatoid arthriti
  • Type-II collagen

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

Cite this

Induction of tolerance against the arthritogenic antigen with type-II collagen peptide-linked soluble MHC class II molecules. / Park, Yoon Kyung; Jung, Sundo; Park, Se-Ho.

In: BMB Reports, Vol. 49, No. 6, 2016, p. 331-336.

Research output: Contribution to journalArticle

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