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Tumor necrosis factor-α (TNF-α) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-α activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-α activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the −383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS ( P = 0.04). The −383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated ( P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype ( P = 0.02). These data suggest that −383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients. [ABSTRACT FROM AUTHOR]

CD28 expression and serum levels are significantly increased in patients with SLE than in healthy controls (HC). Until now, there are no studies of proximal promoter polymorphisms of CD28 gene in SLE. Therefore, our objective was to investigate the polymorphisms present in the proximal promoter of CD28 in a group of SLE and HC and to associate the polymorphisms present with the CD28 serum levels of 40 patients and 40 controls. One hundred and seven patients as well as 108 controls matched by age range and genders were included. The 11 ACR criteria were analyzed on the clinical files, and the proximal promoter region of CD28 gene was analyzed by direct sequencing of a 489-basepair fragment. C28 serum levels (sCD28) were measured by ELISA technique in 40 patients and 40 controls. Only two of the eight reported polymorphisms were found, and they correspond to rs35593994 (-372 A/G) and rs56156157 (-145 -/C). The first had a prevalence of 41 and 36% in patients and controls respectively and the second of 1.4% in both groups. None of these polymorphisms were associated with SLE, and the polymorphism -372 A/G was not associated with the clinical features of disease. Likewise, the association with the sCD28 and the genotypes of -372 A/G polymorphism was not significant. The polymorphisms of the proximal promoter of CD28 are not associated with SLE, and the polymorphism -372 A/G is not associated with the diagnostic criteria of SLE or the sCD28.

CD28 is one of the main activator receptors involved in systemic lupus erythematosus (SLE) pathogenesis, and its expression and serum levels are significantly higher in patients with SLE and other autoimmune diseases than in healthy controls (HC). However, it is unknown whether this increase is associated with specific organ damage. Therefore, our objective was to measure the CD28 levels in serum from SLE and HC groups to confirm the CD28 serum levels increase, as reported previously, and to determine whether this increase was associated with specific organ activity and the SLE Disease Activity Index (SLEDAI). Forty SLE patients and 40 matched HC were included, and the age, disease duration, SLEDAI and Mexican SLEDAI were recorded for the SLE group. CD28 serum levels were measured by ELISA. There was a statistically significant increase in the CD28 serum levels of SLE patients compared to controls (p = 0.039); however, we did not find any significant correlation with disease activity indices or organ involvement, although we found a significant but low correlation with C3. Our results and a review of the literature suggest that the increase in CD28 serum levels may be the result of CD28 gene overexpression, which could be related to the decrease in CD28+ T cells, T-cell hyporesponsiveness and immune impairment that occurs in SLE.

The objective of this study is to establish whether there is an association between the presence of FCGR3A V(176) polymorphism with SLE or its manifestations. We included 94 patients according to the 1982 ACR criteria as well as 98 controls matched by age and gender. The 11 ACR diagnostic criteria were analyzed on the clinical files. The polymorphism FCGR3A V(176) was determined by direct sequencing. There was not an association between the polymorphism FCGR3A V(176) with SLE or its main manifestations. The allelic frequency for F(176) was: 0.80 and 0.72 in cases and controls, respectively (P = 0.09, IC95%: 0.42-1.07); and the genotypic frequency in the group of cases was: 0.65 for homozygotes F(176)/F(176), 0.30 for heterozygotes and 0.05 for the homozygotes V(176)/V(176), while for the control group it was 0.53, 0.39 and 0.08, respectively. The polymorphism FCGR3A V(176) is not associated with SLE or any of its manifestations in patients with SLE from the West of Mexico.

Tumor necrosis factor-alpha (TNF-alpha) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-alpha activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-alpha activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the -383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS (P = 0.04). The -383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated (P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype (P = 0.02). These data suggest that -383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients.