scholarly journals Serum Nerve Growth Factor, Interleukin-13 and Tumor Necrosis Factor - Αin patients with Systemic Lupus Erythematosus

2009 ◽  
Vol 29 (2) ◽  
pp. 151-164
Author(s):  
Magdy Al Tahhan ◽  
Mervat El-Toukhy ◽  
Ehab Salem
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Systemic Lupus ◽  
Nerve Growth ◽  
Interleukin 13 ◽  
Necrosis Factor

Tumor necrosis factor receptor II and PTPN22 genes polymorphisms and the risk of systemic lupus erythematosus in Egyptian children

Lupus ◽  
2021 ◽  
pp. 096120332110203
Author(s):  
Riham Eid ◽  
Ayman Hammad ◽  
Maha Abdelsalam ◽  
Aya Ahmed Fathy ◽  
Dena M Abd-El Ghafaar ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Tumor Necrosis Factor ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Tyrosine Phosphatase ◽  
Tumor Necrosis Factor Receptor ◽  
Clinical Manifestations ◽  
Systemic Lupus ◽  
Egyptian Children ◽  
Necrosis Factor

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.

scholarly journals Tumor Necrosis Factor-α Antagonist Etanercept Decreases Blood Pressure and Protects the Kidney in a Mouse Model of Systemic Lupus Erythematosus

Hypertension ◽  
2010 ◽  
Vol 56 (4) ◽  
pp. 643-649 ◽  
Author(s):  
Marcia Venegas-Pont ◽  
Michaele B. Manigrasso ◽  
Samira C. Grifoni ◽  
Babbette B. LaMarca ◽  
Christine Maric ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Mouse Model ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Systemic Lupus ◽  
Factor Α ◽  
Necrosis Factor

Modification of lymphoid and brain nerve growth factor levels in systemic lupus erythematosus mice

1996 ◽  
Vol 204 (1-2) ◽  
pp. 13-16 ◽  
Author(s):  
Luisa Bracci-Laudiero ◽  
Thomas Lundeberg ◽  
Carina Stenfors ◽  
Elvar Theodorsson ◽  
Paola Tirassa ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Nerve Growth

Adipokines, tumor necrosis factor and its receptors in female patients with systemic lupus erythematosus

Lupus ◽  
2016 ◽  
Vol 26 (1) ◽  
pp. 10-16 ◽  
Author(s):  
F M M Santos ◽  
R W Telles ◽  
C C D Lanna ◽  
A L Teixeira ◽  
A S Miranda ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Damage Index ◽  
Antimalarial Drugs ◽  
Systemic Lupus ◽  
Factor Α ◽  
Necrosis Factor

Objectives To analyze the association of adipokines and tumor necrosis factor α (TNFα) and its receptors with characteristics of systemic lupus erythematosus (SLE) and to investigate the correlation between adipokines and the TNF system. Methods One hundred and thirty-six SLE women, aged ≥18 years old, were assessed. TNFα, soluble TNFα receptors 1 (sTNFR1) and 2 (sTNFR2) and adipokines were analyzed by ELISA kits. Results The median (IQR) of age was 41.5 (33.0–49.7) years old and of disease duration 11.3 (7.8–15.8) years. The median (IQR) of disease activity was 0 (0–4) and of damage index was 2 (1–3). Higher levels of sTNFR1 and sTNFR2 were associated with nephritis ( p < 0.001 for both), and sTNFR1 ( p = 0.025) and TNFα ( p = 0.014) were positively associated with arthritis. Higher sTNFR1 levels were found in participants that were not using antimalarial drugs ( p = 0.04). Independent correlation was found between sTNFR1 (β = 0.253; p = 0.003) and sTNFR2 (β = 0.297; p < 0.001) levels and disease activity and damage index (sTNFR1: β = 0.367; p < 0.001; sTNFR2: β = 0.335; p < 0.001). Higher adiponectin levels were independently associated with nephritis ( p = 0.009) and antimalarial drugs use ( p = 0.015). There was a positive correlation between leptin and sTNFR2 levels ( p = 0.002) and between resistin levels and sTNFR1 ( p < 0.001) and sTNFR2 ( p < 0.001). Conclusion The correlation between adipokines and TNF system allows a better understanding of the role of adipokines in the inflammatory response in SLE patients.

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