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Increased expression of human leucocyte antigen class I free heavy chains on monocytes of patients with spondyloarthritis and cells transfected with HLA ‐ B 27
Author(s) -
Ding Jin,
Feng Yuan,
Zheng Zhao Hui,
Li Xue Yi,
Wu Zhen Biao,
Zhu Ping
Publication year - 2015
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12169
Subject(s) - pathogenesis , transfection , flow cytometry , human leukocyte antigen , immunology , hla b27 , u937 cell , antigen , synovial fluid , microbiology and biotechnology , biology , chemistry , cell culture , medicine , pathology , osteoarthritis , genetics , alternative medicine
Summary Human leucocyte antigen ( HLA )‐ B 27 expression is correlated with spondyloarthritis ( S p A ), but its role in disease pathogenesis remains unclear. The aim of the study was to determine whether HLA ‐B27 free heavy chain ( FHC ) contributes to S p A pathogenesis. Flow cytometry was used to analyse the FHC expression on CD 3+ and CD 14+ cells in the peripheral blood ( PB ) and synovial fluid ( SF ) from SpA patients, healthy controls, and rheumatoid arthritis ( RA ) patients. Human monocytic U937 cell lines stably expressing enhanced green fluorescence protein ( EGFP )/ HLA ‐B27, EGFP / HLA ‐A2 or EGFP alone were created to further investigate the relation between HLA ‐B27 and FHC expression. The relative FHC level on CD 14+ PB cells was significantly higher in SpA patients than in controls, but lower than on the SF cells of SpA patients. No significant correlation was found for relative FHC expression with HLA ‐B27 or β 2‐microglobulin expression. HLA ‐B27‐transfected U937 cells expressed higher FHC levels than either EGFP / HLA ‐A2‐ or EGFP ‐transfected cells. HLA class I FHC expression was significantly increased on monocytes of SpA patients and HLA ‐B27‐transfected cells, implying that FHC , perhaps mostly derived from HLA ‐B27, plays an important role in SpA pathogenesis.