TUMOR NECROSIS FACTOR-α CONVERTING ENZYME EXPRESSION IN THE JOINTS OF RHEUMATOID ARTHRITIS PATIENTS

2002 ◽  
Vol 06 (02) ◽  
pp. 63-71 ◽  
Author(s):  
Koichiro Takahi ◽  
Tetsuya Tomita ◽  
Takanobu Nakase ◽  
Motoharu Kaneko ◽  
Hiroshi Takano ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Subchondral Bone ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mononuclear Cells ◽  
Converting Enzyme ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The purpose of this study is to investigate the expression of tumor necrosis factor-α converting enzyme (TACE) in the synovium and subchondral bone region of patients with rheumatoid arthritis (RA) and to determine the contribution of the enzyme to the pathogenesis of RA. Joint tissues were obtained during total knee arthroplasty from patients with RA and osteoarthritis (OA). The expression of TACE and TNF-α mRNA was detected by in situ hybridization. Characterization of TACE expressing cells was performed by immunohistochemistry using serial sections. We found that TACE mRNA was expressed in both synovium and subchondral bone region and co-localized with TNF-α mRNA in RA. On the other hand, TACE mRNA expression was scarcely detectable in OA samples. TACE was expressed in mononuclear cells, such as CD3 and CD14 positive cells in RA samples. In conclusion, the expression of TACE is up-regulated in the rheumatoid synovium and subchondral bone region, and the results in this study demonstrate that TACE may be involved and play a role in the pathogenesis of RA.

scholarly journals Macrocyclic θ-defensins suppress tumor necrosis factor-α (TNF-α) shedding by inhibition of TNF-α–converting enzyme

2018 ◽  
Vol 293 (8) ◽  
pp. 2725-2734 ◽  
Author(s):  
Justin B. Schaal ◽  
Thorsten Maretzky ◽  
Dat Q. Tran ◽  
Patti A. Tran ◽  
Prasad Tongaonkar ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Converting Enzyme ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor Necrosis Factor-α Inhibitor Use Is Not Associated with Lipid Changes in Rheumatoid Arthritis

2012 ◽  
Vol 39 (5) ◽  
pp. 946-948 ◽  
Author(s):  
ANDRONIKI BILI ◽  
STEPHANIE J. MORRIS ◽  
JENNIFER A. SARTORIUS ◽  
H. LES KIRCHNER ◽  
JANA L. ANTOHE ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Levels ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.To determine the association of use of tumor necrosis factor-α (TNF-α) inhibitors with differences in lipid levels in patients with rheumatoid arthritis (RA).Methods.We studied 807 patients with incident RA to compare differences in lipid levels in TNF-α inhibitor users versus nonusers, with adjustment for relevant covariables.Results.TNF-α inhibitor use was not associated with differences in levels of low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), triglycerides, LDL:HDL, or TC:HDL compared to nonusers.Conclusion.Use of TNF-α inhibitor was not associated with differences in lipid levels in patients with RA.

scholarly journals Granuloma Annulare: a Review of the Literature

2020 ◽  
Vol 24 (4) ◽  
pp. 410-415
Author(s):  
Tânia Aguiar Passeti ◽  
Wesley Pascoal Lisboa ◽  
Gabrielle Ellen Rodrigues Grinblat ◽  
Fernando Luiz Affonso Fonseca ◽  
Paulo Ricardo Criado ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mononuclear Cells ◽  
Granuloma Annulare ◽  
Activation Patterns ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Granuloma annulare (GA) is a form of noninfectious skin granuloma, first described in 1895 as a rash in the form of a ring (annular), with regular, rounded edges. Around 50% of the cases are cured spontaneously within 2 years, however, a percentage of patients suffer from recurrent lesions or persistence for years. The pathogenesis of GA lesions is not well understood, with studies linking its expression to the presence of histocompatibility genes (HLA)-Bw35 or AH8.1 allele. These genes are related to the production of TNF-α (Tumor Necrosis Factor-α) by mononuclear cells. The pathogenesis includes the migration of macrophages to the dermis, the presence of cytokines, late hypersensitivity reaction, defects in regulating the neutrophil chemotaxis and degradation of the connective tissue. Its outbreak may be linked to predisposing factors, such as diabetes mellitus, thyroid changes and viral infectious diseases. The macrophages present in GA lesions may receive stimuli that result in its modulation to M1 or M2 activation patterns. The study of the M1 and M2 modulation mechanism in the lesion is important for an understanding of GA development.   Keywords: Granuloma Annulare. Macrophage. Immunology. Pathogenesis and Modulation.     Resumo O Granuloma Anular (GA) é um tipo de granuloma cutâneo não infeccioso, que foi descrito em 1895, como uma exantema em formato de anel (anular), de bordas regulares e arredondadas. Cerca de 50% dos casos têm cura espontânea em 2 anos, mas parte dos pacientes apresentam recidivas das lesões ou persistência por anos. A patogênese das lesões do GA é pouco conhecida. Estudos relacionam sua expressão à presença de genes de histocompatibilidade (HLA)-Bw35 ou AH8.1, que são relacionados à produção de TNF-α (Tumor necrosis factor - α), pelas células mononucleares. A patogênese também inclui migração de macrófagos para derme, presença de citocinas, reação de hipersensibilidade tardia, defeito na quimiotaxia de neutrófilos e degradação do tecido conectivo. O surgimento das lesões pode estar associado a fatores predisponentes, como diabetes mellitus, alterações tireoidianas e doenças infecciosas virais. Os macrófagos presentes nas lesões de GA podem sofrer estímulos que acarretem sua modulação para os padrões de ativação M1 ou M2. O estudo de tais mecanismo de modulação é importante para a compreensão da instalação e desenvolvimento do GA nos pacientes afetados.   Palavras-chave: Granuloma Anular. Macrófagos. Modulação. Imunologia e Patogênese.

Tumor necrosis factor-α -308 polymorphism in North Indian rheumatoid arthritis patients and association with mRNA and serum TNF-α

2017 ◽  
Vol 36 (10) ◽  
pp. 2209-2216 ◽  
Author(s):  
Mohd Jahid ◽  
Rehan-Ul-Haq ◽  
Puja Kumari Jha ◽  
Diwesh Chawla ◽  
Rajnish Avasthi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Inactive Rhomboid Protein 2 Mediates Intestinal Inflammation by Releasing Tumor Necrosis Factor–α

2019 ◽  
Vol 26 (2) ◽  
pp. 242-253
Author(s):  
Jee Hyun Kim ◽  
Sung Wook Hwang ◽  
Jaemoon Koh ◽  
Jaeyoung Chun ◽  
Changhyun Lee ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Immune Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Inflammation ◽  
Converting Enzyme ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Inactive rhomboid 2 (iRhom2) is an essential molecule required for the maturation of tumor necrosis factor–α–converting enzyme in immune cells, which regulates TNF-α release. The aim of this study was to investigate the role of iRhom2 in intestinal inflammation.

The Risk of Tuberculosis in Patients with Rheumatoid Arthritis Treated with Tumor Necrosis Factor-α Antagonist: A Metaanalysis of Both Randomized Controlled Trials and Registry/Cohort Studies

2015 ◽  
Vol 42 (12) ◽  
pp. 2229-2237 ◽  
Author(s):  
Jing-Wen Ai ◽  
Shu Zhang ◽  
Qiao-Ling Ruan ◽  
Yi-Qi Yu ◽  
Bing-Yan Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Cohort Studies ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Controlled Trials ◽  
Randomized Controlled ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.Tumor necrosis factor-α (TNF-α) antagonists have significantly improved treatment results in rheumatoid arthritis (RA), but have also increased the risk of tuberculosis (TB). Etanercept (ETN), adalimumab (ADA), infliximab (IFX), golimumab, and certolizumab pegol are the 5 drugs currently available on the market. This article aimed to evaluate the risk of TB infection from these 5 drugs for patients with RA.Methods.We searched PubMed, EMBASE, COCHRANE library, OVID, and EBSCO for randomized controlled trials (RCT) of TNF-α antagonist versus control and registry/longitudinal cohort studies of 1 TNF-α antagonist versus another. The Mantel-Haenszel test was adopted to analyze risk ratio (RR) in this metaanalysis.Results.Fifty RCT and 13 non-RCT were included in this study. No significant difference in TB risk was found in the RCT because of the short observational periods. In the non-RCT, TNF-α antagonist was associated with a higher TB risk in patients with RA (RR 4.03, 95% CI 2.36–6.88), and the TB incidence rates of IFX and ADA were 2.78 and 3.88 times, respectively, higher than that of ETN. Further, preventive treatment for latent TB infection (LTBI) was shown to reduce the TB risk by 65% (RR 0.35, 95% CI 0.15–0.82).Conclusion.This study demonstrated a significant increase in TB risk in patients with RA treated with TNF-α antagonists; among them, ETN is least likely to cause active TB. The study also proposes the necessity of LTBI prophylaxis in patients with RA.

Disease Activity Improvement in Rheumatoid Arthritis Treated with Tumor Necrosis Factor-α Inhibitors Correlates with Increased Soluble Fas Levels

2014 ◽  
Vol 41 (10) ◽  
pp. 1961-1965 ◽  
Author(s):  
Eloisa Romano ◽  
Riccardo Terenzi ◽  
Mirko Manetti ◽  
Francesca Peruzzi ◽  
Ginevra Fiori ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Soluble Fas ◽  
Tnf Α ◽  
Before And After ◽  
Factor Α ◽  
Necrosis Factor

Objective.Rheumatoid arthritis (RA) is characterized by chronic synovial inflammation and hyperplasia. Tumor necrosis factor-α (TNF-α) plays a pivotal role in RA by interfering with the Fas–Fas ligand (FasL) proapoptotic pathway. We investigated the circulating levels of soluble Fas (sFas) and soluble FasL (sFasL), and their possible correlation with disease activity and improvement after anti-TNF-α treatment in RA.Methods.Serum levels of sFas and sFasL were measured by quantitative ELISA in 52 patients with RA before and after 3 months of anti-TNF-α treatment (adalimumab, n = 32; infliximab, n = 20). Disease activity measures [Disease Activity Score at 28 joints-erythrocyte sedimentation rate (DAS28-ESR), C-reactive protein (CRP)] were recorded before and after treatment. Forty age-matched and sex-matched healthy subjects served as controls.Results.No significant differences in serum sFas levels were detected between anti-TNF-α-naive patients with RA and controls. After anti-TNF-α treatment, serum sFas levels significantly increased in patients with RA compared to both anti-TNF-α-naive patients and controls. Increased sFas levels inversely correlated with disease activity variables (DAS28-ESR: r = −0.739, CRP: r = −0.636, both p < 0.001). No significant differences in sFasL levels were detected in patients with RA before and after anti-TNF-α treatment.Conclusion.In RA, an increase in sFas levels closely correlates with improvement in disease activity induced by TNF-α inhibitors, suggesting their ability to modulate Fas-mediated synoviocyte apoptosis.

scholarly journals P2X7 Receptor Induces Tumor Necrosis Factor-α Converting Enzyme Activation and Release to Boost TNF-α Production

2017 ◽  
Vol 8 ◽  
Author(s):  
Maria Barberà-Cremades ◽  
Ana I. Gómez ◽  
Alberto Baroja-Mazo ◽  
Laura Martínez-Alarcón ◽  
Carlos M. Martínez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
P2x7 Receptor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Enzyme Activation ◽  
Converting Enzyme ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor
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