YERSINIA-ENTEROCOLITICA SEROTYPE O-3 ALTERS THE EXPRESSION OF SEROLOGIC HLA-B27 EPITOPES ON HUMAN MONOCYTES

Citation
M. Wuorela et al., YERSINIA-ENTEROCOLITICA SEROTYPE O-3 ALTERS THE EXPRESSION OF SEROLOGIC HLA-B27 EPITOPES ON HUMAN MONOCYTES, Infection and immunity, 65(6), 1997, pp. 2060-2066
Citations number
52
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
65
Issue
6
Year of publication
1997
Pages
2060 - 2066
Database
ISI
SICI code
0019-9567(1997)65:6<2060:YSOATE>2.0.ZU;2-I
Abstract
The expression of serologic HLA-B27 epitopes on leukocytes of patients with reactive arthritis or ankylosing spondylitis has been shown to b e modified in the course of the disease. The purpose of this work was to study whether phagocytosis of arthritis-triggering microbes in vitr o alters the expression of HLA-B27 molecules on human antigen-presenti ng cells and to characterize the underlying mechanisms. Human monocyte s and HLA-B27- or HLA-A2-transfected human U-937 cells were exposed to Yersinia enterocolitica serotype 0:3. The expression of different epi topes of HLA-B27 was monitored by using immunofluorescence, and their synthesis was determined by quantitative immunoprecipitation. Our resu lts show that phagocytosis of Y. enterocoalitica serotype 0:3 changed the expression of serological HLA-B27 epitopes. This was due to the re duced synthesis of HLA-B27 molecules. The expression of especially the epitopes which depend on the presence of peptides in the antigen-bind ing groove was changed. The expression of the ME1 epitope, which has b een shown to be important for- T-cell recognition in patients with rea ctive arthritis, was decreased. Down-regulation of epitopes important for the T-cell recognition may impair the elimination of arthritis-tri ggering microbes and lead to persistent infection. In addition, Y. ent erocolitica serotype 0:3 seemed to alter the repertoire of peptides pr esented by the HLA-B27 molecules on human monocytes. This may have a r ole in the pathogenesis of reactive arthritis via an autoimmune mechan ism.