Increased expression of Toll‐like receptor 4 in peripheral blood leucocytes and serum levels of some cytokines in patients with ankylosing spondylitis
Author(s) -
Yang Z.X.,
Liang Y.,
Zhu Y.,
Li C.,
Zhang L.Z.,
Zeng X.M.,
Zhong R.Q.
Publication year - 2007
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2007.03396.x
Subject(s) - proinflammatory cytokine , tlr4 , immunology , tumor necrosis factor alpha , ankylosing spondylitis , medicine , immune system , erythrocyte sedimentation rate , tlr2 , receptor , toll like receptor , interleukin 6 , pathogenesis , inflammation , innate immune system
Summary Toll‐like receptor 4 (TLR4) is a member of the Toll‐like receptor family, which can bridge innate and adaptive immune responses. Activation of the TLR4 signalling pathway may induce the release of proinflammatory cytokines such as tumour necrosis factor (TNF)‐α and interleukin (IL)‐12, which was considered to play an important role in pathogenesis of immune‐mediated diseases. Ankylosing spondylitis (AS) is an immune‐mediated disease whose aetiology remains unknown. The aim of the study was to investigate the expression of TLR4 and serum TNF‐α, IL‐12 and soluble tumour necrosis factor‐related apoptosis‐inducing ligand (sTRAIL) level in AS patients. The results indicated that TLR4 protein and mRNA levels were significantly higher in AS patients than in healthy controls; however, there was no significant difference between human leucocyte antigen (HLA)‐B27‐positive and ‐negative AS patients, as well as serum levels of TNF‐α, IL‐12 and sTRAIL. In addition, in HLA‐B27‐positive AS patients, TLR4 level showed close associations with the cytokines and laboratory parameters of disease activity [erythrocyte sedimentation rate (ESR) and plasma C‐reactive protein (CRP)], respectively. Similarly, the strong associations between the cytokines or between IL‐12 and ESR or CRP were observed in HLA‐B27‐positive AS patients. Interestingly, in HLA‐B27‐positive AS patients, TNF‐α correlated significantly with ESR, but did not with CRP. In contrast, sTRAIL correlated with CRP, but did not with ESR. Among HLA‐B27‐negative patients, no close correlation was found. In our study, it was suggested that the abnormal activation of TLR4 signalling and serum TNF‐α, IL‐12 and sTRAIL may play a key role in the development and progression of AS, which may be dependent on the status of HLA‐B27 antigen.
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