Showing 4 results for Rheumatoid Arthritis
Golnesa Dadkhah, Hadi Bazzazi, Yaghoub Yazdani,
Volume 6, Issue 3 (9-2018)
Abstract
Background and objectives: Rheumatoid arthritis (RA) is a complex and systemic inflammatory disease in which the immune response is disturbed. Single nucleotide polymorphisms (SNPs) in the promoter regions of regulatory cytokines including interleukin-10 (IL-10) may lead to exacerbated immune response and increased risk of RA. Here, we aimed to assess the association of IL-10 -1082 (G/A) (rs1800896) promoter polymorphism with the susceptibility to RA in a population in northeast of Iran.
Methods: A total of 130 RA patients and 128 sex- and age- matched healthy donors were enrolled. The polymerase chain reaction (PCR) was used to amplify the polymorphic regions and restriction fragment length polymorphism (RFLP) technique was applied to detect rs1800896. SPSS 22.0 software was used to analyze data statistically.
Results: Our findings revealed that G allele was significantly associated with the increased risk of RA [OR = 1.88, 95% CI (1.32–2.66), P-value = 0.0001] in patients. Setting AA genotype as the reference, the AG [OR = 2.93, 95% CI (1.68–5.12), P-value = 0.0001] and GG [OR = 5.73, 95% CI (2.30–14.23), P-value = 0.0001] genotypes were significantly associated with RA susceptibility.
Conclusion: The present study suggests that the IL-10 -1082 (G/A) genetic variants are associated with RA susceptibility, but not with the disease activity. While this is the first time to report such an association in a population in northeast of Iran, further studies are needed to confirm these findings.
Sahar Ghovanjzadeh, Hadi Bazzazi, Yaghoub Yazdani,
Volume 6, Issue 3 (9-2018)
Abstract
Background and objectives: Rheumatoid arthritis (RA) is an autoimmune disease with a complex genetic background. The protein tyrosine phosphatase non-receptor type 22 (PTPN22) is a lymphoid specific protein tyrosine phosphatase which is involved in negative regulation of T cell response. Several studies have assessed the association between PTPN22 single nucleotide polymorphisms (SNPs) with RA susceptibility. Here, we aimed to assess the association of PTPN22 (1858 C>T) variant with the susceptibility to RA in northeast of Iran.
Methods: A total of 127 RA patients and 119 age- and sex- matched healthy donors were enrolled. The polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) technique (PCR-RFLP) was applied to detect PTPN22 (1858 C>T) SNP. SPSS 22.0 software was used to analyze data using relevant statistical tests.
Results: Comparison of allele and genotype frequencies of PTPN22 (1858 C>T) SNP in RA patients and healthy donors revealed no significant association with RA susceptibility.
Conclusion: The present study suggests that the PTPN22 (1858 C>T) genetic variants are not associated with RA susceptibility and disease activity. While this is the first report from northeast of Iran, further studies are needed to confirm these findings
Faezeh Ajam, Mehrdad Aghaei, Saeed Mohammadi, Mohsen Saeedi, Nasser Behnampour, Ali Memarian,
Volume 7, Issue 2 (7-2019)
Abstract
Study objectives: Rheumatoid arthritis (RA) is a common chronic and systemic autoimmune disease, characterized by inflammation and the destruction of the joints. It is well known that CD4+ T cells play a major role in the pathogenesis of RA. Expanded subpopulations of CD4+ T cells have been reported in RA patients. Here, we investigated the expression of PD-1 on subsets of CD4+ T cells (CD4+CD28- and CD4+CD28+ T cells) in the peripheral blood (PB) and synovial fluid (SF) of patients with RA.
Methods: A total of 42 RA patients, including 10 newly diagnosed (ND) and 32 relapsed (RL) cases and also 20 healthy controls were enrolled. Phenotypic characterization subsets of CD4+ T cells were evaluated by flow cytometry, using fluorescence conjugated specific human monoclonal antibodies.
Results: The frequency of CD4+CD28+ T cells was significantly increased in SF versus PB in ND and RL patients. In contrast, the percentage of CD4+CD28- T cells was elevated in PB of ND and RL patients comparison to SF. Expression of PD-1 on CD4+CD28+ and CD4+CD28- T cells in PB of ND and RL patients was significantly higher than the healthy controls. Furthermore, PD-1 expression on CD4+CD28+ and CD4+CD28- T cells in SF versus PB of RL patients were significant increased.
Conclusion: These data suggest that CD4+ T cells subsets in RA patients were resistance to PD-1 mediated effects and PD-1 has insufficient ability to suppression of CD4+T cells.
Nafiseh Kaviani, Yaghoub Yazdani, Hadi Bazzazi,
Volume 7, Issue 4 (12-2019)
Abstract
Background and objectives: Vitamin D receptor (VDR) has been identified as a susceptibility gene for several autoimmune diseases. This study was designed to investigate the association of VDR gene polymorphisms with the susceptibility to rheumatoid arthritis (RA).
Methods: A case-control study was performed on 130 RA patients and 128 healthy subjects in the north-east of Iran using restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) technique.
Results: Our findings suggested a significant association of T allele (p=0.01) of TaqI (rs731236), and f allele (p=0.01) of FokI (rs10735810) genetic variants of the VDR gene with RA susceptibility. These significant associations were also found in the T/T genotype of TaqI (p=0.009), and F/f genotype of FokI (P=0.014). The f-T haplotype was more significantly detected in-patients than in healthy controls (p=0.007).
Conclusion: The RA group showed an increase in the f allele and heterozygous F/f genotype and also in the T allele and homozygous T/T and heterozygous T/t genotypes as compared to the control group. Our results demonstrated that polymorphisms of TaqI and FokI in the VDR gene might be involved in the development of RA in an Iranian population.
