Spontaneous inflammatory disease in HLA-B27 transgenic mice does not require transporter of antigenic peptides

Sanjay D. Khare, S. Lee, M. J. Bull, J. Hanson, H. S. Luthra, C. S. David

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

HLA-B27 is strongly linked with a group of human diseases called spondylearthropathies. Even though HLA-B27 as an MHC class I molecule would be expected to present endogenously processed peptides such as cytosolic or viral proteins, many of the B27-linked diseases begin after an infection with an enterobacteria, an exogenous antigen. In our previous studies, we have described development of spontaneous inflammatory disease in HLA-B27 transgenic mice expressing β2m free heavy chains on the cell surface. In order to address the role of endogenous versus exogenous antigens and a role for Tap genes in the development of spontaneous diseases, mice lacking Tap-1 (knockout) were mated to HLA-B27/human β2m transgenic mice. B27+/human β2m+ double-transgenic mice (without mouse β2m) lacking the Tap-1 gene developed spontaneous inflammatory disease similar to wild-type Tap-1 gene-expressing counterparts. Our data demonstrate that peptide transporters (Tap) were not involved in the development of spontaneous inflammatory disease in B27+/human β2m transgenic animals.

Original languageEnglish (US)
Pages (from-to)364-369
Number of pages6
JournalClinical Immunology
Volume98
Issue number3
DOIs
StatePublished - Jan 1 2001

Keywords

  • Endogenous peptides
  • HLA-B27
  • Reactive arthritis
  • Spondyloarthropathy
  • TAP polymorphism

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Spontaneous inflammatory disease in HLA-B27 transgenic mice does not require transporter of antigenic peptides'. Together they form a unique fingerprint.

  • Cite this