The frequencies of inhibitory KIR2DL2 and KIR2DL5 were significantly lower in the ReA patients than in the controls (p = .005 and p = .033, respectively).
The frequencies of inhibitory KIR2DL2 and KIR2DL5 were significantly lower in the ReA patients than in the controls (p = .005 and p = .033, respectively).
Moreover, we found that activating KIR2DS1 alone or in combination with the HLA-C1C1 genotype (which indicates the absence of the HLA ligands for their homologous inhibitory receptor KIR2DL1) is associated with susceptibility to ReA (p = .039 and p = .011, respectively), whereas KIR2DL2 in combination with the HLA-C1 ligand is associated with protection against ReA (p = .039).
Moreover, we found that activating KIR2DS1 alone or in combination with the HLA-C1C1 genotype (which indicates the absence of the HLA ligands for their homologous inhibitory receptor KIR2DL1) is associated with susceptibility to ReA (p = .039 and p = .011, respectively), whereas KIR2DL2 in combination with the HLA-C1 ligand is associated with protection against ReA (p = .039).
Moreover, we found that activating KIR2DS1 alone or in combination with the HLA-C1C1 genotype (which indicates the absence of the HLA ligands for their homologous inhibitory receptor KIR2DL1) is associated with susceptibility to ReA (p = .039 and p = .011, respectively), whereas KIR2DL2 in combination with the HLA-C1 ligand is associated with protection against ReA (p = .039).
<b>Conclusion:</b> Our studies show that CTHRC1 is a sensitive and easy-to-measure plasma marker that differentiates between RA and healthy status and also distinguishes between RA and other forms of arthritis, such as OA and ReA.
Serum cathepsin K and C-reactive protein were higher in ReA patients compared to controls (p = 0.03 for both), while total cholesterol and low-density lipoprotein were lower (p = 0.008 and 0.045, respectively).
Our report supports previous literature data of possible overlap existing between RA and SpA, but also presents for the first time the association of high titers of anti-CCP antibodies with SII and reactive arthritis in patients with no peripheral small joint involvement.
IL-17 and IFN-γ producing NK and γδ-T cells are preferentially expanded in synovial fluid of patients with reactive arthritis and undifferentiated spondyloarthritis.
IL-17 and IFN-γ producing NK and γδ-T cells are preferentially expanded in synovial fluid of patients with reactive arthritis and undifferentiated spondyloarthritis.
To evaluate the status of total IgA and SIgA, and the association among the levels of SIgA, IgA, IgA anti-<i>Chlamydia trachomatis</i>, and anti-<i>Shigella</i> spp. with the disease activity measures, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels, was compared in a cohort of patients with ReA and uSpA and healthy subjects.
Thus, OmpA of S. typhimurium is a target of SF CD8(+) T cells and drives SFMC to produce increased cytokines of the IL-17/IL-23 axis which contribute to the pathogenesis of Salmonella-triggered ReA.
Recombinant Salmonella typhimurium outer membrane protein A is recognized by synovial fluid CD8 cells and stimulates synovial fluid mononuclear cells to produce interleukin (IL)-17/IL-23 in patients with reactive arthritis and undifferentiated spondyloarthropathy.
The attack rate of CiReA in our study was higher than previously reported, but the CCR5-delta-32 mutation does not seem to play a role in CiReA disease susceptibility.
Polymerase chain reaction (PCR) defined CCR5 genotype in synovial tissue DNA from 218 individuals: 21 controls, 110 with reactive arthritis (ReA), 83 with undifferentiated oligoarthritis (UO), 4 with osteoarthritis (OA).Disease durations were 0.5 to 21 years.
There was a remarkably high proportion of proangiogenic factors, in particular IP10, ENA-78, and IL-8 accounting for a genetically determined susceptibility to ReA at the host cell level.
There was a remarkably high proportion of proangiogenic factors, in particular IP10, ENA-78, and IL-8 accounting for a genetically determined susceptibility to ReA at the host cell level.
Campylobacter or Salmonella infection in women, use of proton pump inhibitors and an SNP in the IFNG gene were independent risk factors for reactive arthritis.