Autoantibodies to Tumor Necrosis Factor in Patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus

2009 ◽  
Vol 36 (4) ◽  
pp. 753-756 ◽  
Author(s):  
BARBARA J. ROSENAU ◽  
PETER H. SCHUR

Objective.To detect autoantibodies to tumor necrosis factor (TNF) in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), and to determine their clinical correlates.Methods.Ninety-two patients with RA and 62 with SLE were studied. Sera were examined for autoantibodies to TNF by enzyme linked immunoassay. Levels of these autoantibodies were analyzed in respect to markers of inflammation such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and joint erosions, as well as other clinical, laboratory, and therapeutic aspects of RA and SLE.Results.Anti-TNF levels were higher in those RA patients without erosions, but did not correlate with ESR or CRP.Conclusion.These observations suggest that autoantibody anti-TNF may be part of the innate immune system and may contribute to decreased inflammation in patients with RA.

2021 ◽  
Vol 22 (8) ◽  
pp. 4095
Author(s):  
Neža Brezovec ◽  
Katja Perdan-Pirkmajer ◽  
Saša Čučnik ◽  
Snežna Sodin-Šemrl ◽  
John Varga ◽  
...  

Deregulation of adiponectin is found in systemic autoimmune rheumatic diseases (SARDs). Its expression is downregulated by various inflammatory mediators, but paradoxically, elevated serum levels are present in SARDs with high inflammatory components, such as rheumatoid arthritis and systemic lupus erythematosus. Circulating adiponectin is positively associated with radiographic progression in rheumatoid arthritis as well as with cardiovascular risks and lupus nephritis in systemic lupus erythematosus. However, in SARDs with less prominent inflammation, such as systemic sclerosis, adiponectin levels are low and correlate negatively with disease activity. Regulators of adiponectin gene expression (PPAR-γ, Id3, ATF3, and SIRT1) and inflammatory cytokines (interleukin 6 and tumor necrosis factor α) are differentially expressed in SARDs and could therefore influence total adiponectin levels. In addition, anti-inflammatory therapy could also have an impact, as tocilizumab treatment is associated with increased serum adiponectin. However, anti-tumor necrosis factor α treatment does not seem to affect its levels. Our review provides an overview of studies on adiponectin levels in the bloodstream and other biological samples from SARD patients and presents some possible explanations why adiponectin is deregulated in the context of therapy and gene regulation.


Lupus ◽  
2021 ◽  
pp. 096120332110203
Author(s):  
Riham Eid ◽  
Ayman Hammad ◽  
Maha Abdelsalam ◽  
Aya Ahmed Fathy ◽  
Dena M Abd-El Ghafaar ◽  
...  

Background Many genes have been implicated in the pathogenesis of systemic lupus erythematosus (SLE). Tumor necrosis factor (TNF) is a potent cytokine stimulator acting through 2 cell surface receptors (TNFR I and II). TNFRII gene which controls expression of these receptors has been linked to SLE susceptibility through promoting apoptosis. Also; Protein tyrosine phosphatase non receptor 22 (PTPN22) gene enhances intrinsic phosphatase activity of T lymphocytes leading to their dysregulation and stimulates autoimmune process of lupus and its rs2476601 has been linked to susceptibility to thyroiditis in SLE patients in few studies. Objectives (i) to investigate the correlation between 2 SNPs of TNFR II and PTPN22 genes and SLE susceptibility in a cohort of Egyptian children compared to controls (ii) and to investigate their possible association with different clinical presentations of the disease in children. Subjects and methods Typing of TNFR II rs1061622 and PTPN22 rs2476601 SNPs were done using polymerase chain reaction-restriction fragment length polymorphism for 74 children with SLE and 100 matched healthy controls. Results Children with SLE had more frequent G allele and GG genotype of TNFR II rs1061622 ( p < 0.001) and more T allele and TT genotype of PTPN22 rs2476601 ( p = 0.012 and <0.001, respectively) compared to controls. Only 6 patients (8%) had thyroiditis (hypothyroidism) with T allele and TT genotype of PTPN22 1858 T more prevalent in those patients versus those without thyroiditis ( p ≤ 0.001). Apart from, thyroiditis, no significant association was found between genotypes and alleles frequencies of the 2 studied SNPs and other clinical manifestations of the disease. Conclusion The G allele and GG genotype of TNFR II rs1061622 and T allele and TT genotype of PTPN22 rs2476601 genes polymorphism can be considered as risk factors for the development of SLE. The presence of the T allele of PTPN22 rs2476601 may increase the risk of concomitant thyroiditis in Egyptian children with SLE but further studies are required to confirm this finding as thyroiditis was reported only in few cases in this study.


Hypertension ◽  
2010 ◽  
Vol 56 (4) ◽  
pp. 643-649 ◽  
Author(s):  
Marcia Venegas-Pont ◽  
Michaele B. Manigrasso ◽  
Samira C. Grifoni ◽  
Babbette B. LaMarca ◽  
Christine Maric ◽  
...  

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