Serum IL-1β concentrations were significantly elevated in patients with PR, and a splice variant of PYCARD/ ASC mRNA lacking exon 2 (Δexon2) was dominantly expressed compared with that in controls.
To investigate the association between tumour necrosis factor-alpha (TNFalpha), TNF receptor superfamily member 1A (TNFRSF1A, also known as TNFRI), TNFRSF1B (TNFRII), and interleukin-1beta (IL-1beta) single nucleotide polymorphisms (SNPs) and the susceptibility to persistent palindromic rheumatism (PR).
We analyzed the inflammasome adapter PYD and CARD domain-containing protein/apoptosis-associated speck-like protein containing a CARD (PYCARD/ASC) in Japanese patients with PR.
PR patients had a lower frequency of fine ACPA specificities than RA patients, which was significant in the case of a peptide derived from vimentin (PR 24.1% vs. 59.3% RA; p < 0.001).
Compared with the controls, differences in the frequency of single-nucleotide polymorphism (SNP) on padi4_104 [T(RA susceptible)-->C(RA non-susceptible)] and the presence of an RA susceptible homozygote of the PADI4 haplotype were detected in patients with PR whereas we could not find any further difference in PR patients who developed RA compared to PR patients who do not develop RA in PADI4.
Anti-cyclic citrullinated peptide (anti-CCP) antibodies, joint involvement pattern, genotypes of HLA-DRB1, peptidylarginine deiminase (PADI4), and protein tyrosine phosphatase (PTPN22) were examined in 28 patients with PR at baseline, and their clinical outcome was prospectively evaluated.
Cox regression analysis revealed that anti-CCP antibodies as well as PIP involvement are the most relevant variables for the development of RA from PR.
Anti-cyclic citrullinated peptide (anti-CCP) antibodies, joint involvement pattern, genotypes of HLA-DRB1, peptidylarginine deiminase (PADI4), and protein tyrosine phosphatase (PTPN22) were examined in 28 patients with PR at baseline, and their clinical outcome was prospectively evaluated.
The frequency of TNFRSF1B +676T/+1663A was increased in PR patients (OR = 2.12, p = 0.01), but failed to reach statistical significance after Bonferroni correction.
The results of this study provide evidence of an association between persistent PR and SNPs within the TNFRSF1A gene, and suggest that TNFRI is involved in the aetiopathogenesis of PR.