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Increased T‐cell turnover is associated with spondyloarthritis in virally suppressed patients with HIV‐1 infection
Objectives Spondyloarthritis (SpA) is one of the most frequently observed inflammatory joint diseases in HIV‐1‐seropositive patients. T‐cells were described frequently as one of the major driving forces in SpA, therefore we tried to look for T‐cell aberrancies in our HIV‐positive patients with SpA....
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Published in: | HIV medicine 2015-04, Vol.16 (4), p.255-260 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Objectives
Spondyloarthritis (SpA) is one of the most frequently observed inflammatory joint diseases in HIV‐1‐seropositive patients. T‐cells were described frequently as one of the major driving forces in SpA, therefore we tried to look for T‐cell aberrancies in our HIV‐positive patients with SpA.
Methods
A total of 1098 files for HIV‐positive patients who attended the HIV out‐patient clinic of the Department of Clinical Immunology and Rheumatology at the Medical University Hanover for at least one visit between January 2004 and December 2010 were screened for the presence of a diagnosis of SpA. A cross‐sectional study was conducted to investigate aberrancies in T‐cell homeostasis induced by HIV‐1 in these subjects.
Results
The prevalence of SpA in the HIV‐positive patients was 1.6% (18 of 1098). Interestingly, the percentage of patients with SpA who were human leucocyte antigen (HLA)‐B27 negative in our HIV‐positive cohort was 80%. Despite combination antiretroviral therapy (cART) and viral suppression, an incomplete immune recovery of T‐cell naïve/memory distribution and turnover, as identified by intracellular Ki‐67 expression, was observed in HIV‐positive patients with SpA.
Conclusions
Independent of HLA‐B27 status and despite cART, HIV‐positive patients can develop SpA and exhibit an increased T‐cell turnover rate. |
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ISSN: | 1464-2662 1468-1293 |
DOI: | 10.1111/hiv.12199 |