Toll like receptor 9 (TLR 9) expression in peripheral blood mononuclear cell (PBMCs) from treated and untreated Grave’s disease patients

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Ashraf M Okba ◽  
Rasha Y Shaheen ◽  
Gehan M. H Mostafa ◽  
Hanan M Ali ◽  
Sylvia W Abo El Fadle ◽  
...  

Abstract Background It is well known that Autoimmune thyroid disease is multifactorial with multiple genetic and environmental factors, immune malfunction also incriminated in the development of this disease, The exact pathogenesis of this disease remains unclear despite the fact that the production of autoantibodies destroys self-tolerance and agitate the adaptive immune system. Our study will answer the question is there a difference in Toll like receptor 9 (TLR 9) expression in peripheral blood mononuclear cell (PBMCs) from Grave’s disease patients. Objective to measure TLR9 percentage expression on peripheral blood mononuclear cells in patients with Graves’ disease. Methods 60 subjects were included in this study; 30 with Graves’ disease and 30 healthy individuals as control group. All the patients were subjected to the following: Full history, clinical examination, thyroid functions, Thyroid ultrasound, Radioisotope thyroid scan: to assess uptake of thyroid gland and Toll like receptor 9 (TLR 9) percentage expression on peripheral blood mononuclear cells will be analyzed using flow cytometry technique. Results The present study proved that patients with Graves’ disease had higher levels of percentage expression of TLR 9 on peripheral blood lymphocytes. Conclusion percentage expression of TLR9 on peripheral blood lymphocytes is higher in Graves’ patients.

2019 ◽  
Vol 14 (04) ◽  
pp. 149-154
Author(s):  
Hasan Azem Karabacak ◽  
Ozge Yilmaz ◽  
Ibrahim Tuglu ◽  
Fatma Taneli ◽  
Suheyla Surucuoglu ◽  
...  

Background Identification of the immune response against tuberculosis is vital to develop new diagnostic and therapeutic modalities. The objective of this study was to determine IL (interleukin)-18 and IL-27 responses of peripheral blood mononuclear cells to early secreted antigen (ESAT-6) and culture filtrate protein-10 (CFP-10) stimulation in children with a (+) or (−) tuberculin skin test (TST) with in-house tuberculosis contact. Methods We enrolled 40 children aged 1 to 5 years who had an in-house contact with a tuberculous adult. Blood samples were obtained from all children for QuantiFERON tuberculosis (TB) gold in tube (QFT-GIT), and peripheral blood mononuclear blood cell culture tests. The subjects were grouped as TST (−) QFT-GIT (−), TST (+) QFT-GIT (−), and TST (+) QFT-GIT (+). Supernatant of peripheral blood mononuclear cell culture was separated with and without stimulation of ESAT-6 and CFP-10, and IL-18 and IL-27 levels were measured with enzyme linked immunoassay (ELISA) test. Results The study group included 22 boys and 18 girls with mean age 4.25 ± 0.9 years. IL-18 and IL-27 levels were statistically significant in ESAT-6/CFP-10-stimulated supernatants of peripheral blood mononuclear cell (PBMC) samples among the three groups (p = 0.000, p = 0.007, respectively). IL-18 levels between the TST (−) QFT-GIT (−) and TST (+) QFT-GIT (+) groups were significantly different (p = 0.026). Both IL-18 and IL-27 levels were significantly different between ESAT-6/CFP-10 stimulated PBMC supernatants of TST (−) QFT-GIT (−) and TST (+) QFT-GIT (−) groups (p = 0.000, p = 0.003, respectively). Conclusion Low IL-18 and IL-27 responses of peripheral blood mononuclear cells in children with Bacillus Calmette–Guérin (BCG) vaccine may play a role in Mycobacterium tuberculosis infection after in-house contact.


2000 ◽  
Vol 9 (3-4) ◽  
pp. 189-191
Author(s):  
Neville A. Punchard ◽  
John Cason ◽  
Jonathan Mullins ◽  
Chaman Chander ◽  
Richard P. H. Thompson

Basal, lipopolysaccharide (LPS) and silica-stimulated prostaglandin (PG) production were compared between peripheral blood mononuclear cells (PBMNC) from UC patients and healthy subjects (HS). Basal and LPS-stimulated PBMNC PGI2, but not PGE2, production was greater in UC. LPS stimulated both PGE2and PGI2by PBMNC from HS and UC patients. Silica stimulated production of both PGs by cells from HS but only PGE2by cells from UC patients. The differences in responses to silica and LPS may result from differences in activation of NFκB or, alternatively, prior sensitisation to one of these agents. That PBMNC PGE2production is not increased in UC, as it is in Crohn’s disease, suggests that there are differences in PBMNC behaviour between these two diseases.


1995 ◽  
Vol 132 (2) ◽  
pp. 175-180 ◽  
Author(s):  
Mónica Marazuela ◽  
Juan A Vargas ◽  
Melchor Alvarez-Mon ◽  
Fernando Albarrán ◽  
Tomás Lucas ◽  
...  

Marazuela M, Vargas JA, Alvarez-Mon M, Albarrán F, Lucas T, Durántez A. Impaired natural killer cytotoxicity in peripheral blood mononuclear cells in Graves' disease. Eur J Endocrinol 1995;132:175–80. ISSN 0804–4643 We studied the natural killer (NK) activity of peripheral blood mononuclear cells (PBMC) in patients with Graves' disease (GD). Peripheral blood mononuclear cells from 20 untreated hyperthyroid patients with GD showed a significantly reduced NK activity against 51 Cr-labeled K562 cells (33.9 ± 15.9%), while in 32 euthyroid patients under antithyroid drug therapy, NK activity was similar to that of controls (46.9 ± 17.3 and 49.9 ± 20.2%, respectively). Furthermore, normalization of thyroid function with antithyroid drugs was associated with a significant increase and normalization of NK activity during the follow-up of nine GD patients (from 29.2 ± 17.9 to 48.1 ± 16.5%). This phenomenon could not be ascribed to a defective number of NK cells because the amounts of CD56 + and CD16 + cells in PBMC from both hyperthyroid and euthyroid GD patients were within normal ranges. Natural killer activity of PBMC from patients with toxic multinodular goiter was similar to that of normal controls (45 ± 12.8 to 49.9 ± 20%). No correlation was found between natural killer activity and serum levels of free thyroxine, TSH-inhibitory immunoglobulins, thyroidal antibodies to thryoglobulin and thyroidal microsomal antigen, dose or duration of antithyroid drug therapy. Natural killer activity from both controls and GD patients was enhanced in vitro by addition of recombinant interleukin 2 (IL-2), reaching control levels in hyperthyroid patients. These abnormalities were not associated with a defective IL-2 production by T cells, nor with a decreased IL-2R expression. We conclude that in untreated Graves' disease there is a decrease in NK cell activity in PBMC, probably dependent on the autoimmune process. Possible biological and clinical implications are discussed. Monica Marazuela, Hospital de la Princesa, c/Diego de Léon 62, Madrid 28006, Spain


2011 ◽  
Vol 96 (11) ◽  
pp. E1866-E1870 ◽  
Author(s):  
Lingyan Xu ◽  
Xinran Ma ◽  
Yanyan Wang ◽  
Xiaoli Li ◽  
Yicheng Qi ◽  
...  

Abstract Context: Graves' disease (GD) is a common autoimmune disease that affects the thyroid gland. Its pathogenesis is tightly involved with aberrant proinflammatory cytokine production. Osteopontin (OPN), an extracellular matrix protein of pleiotropic properties, has recently been recognized as a potent inflammatory cytokine in several autoimmune diseases. Objective: This study sought to explore the pathophysiological role of OPN in GD by comparing OPN levels in initial GD patients and healthy controls. Methods: Seventy-six patients who met criteria for initial GD and sixty-five healthy controls were recruited. OPN and other clinical GD diagnosis parameters were measured. In addition, the coexpression of several OPN receptors as well as various nuclear factor-κB (NF-κB) downstream target genes were examined in peripheral blood mononuclear cells from human subjects. The effect of OPN on NF-κB activation was determined by in vitro assays. Results: We demonstrated for the first time that the OPN levels are enhanced in serum from GD patients. OPN levels are strongly associated with clinical serum parameters for GD diagnosis. The coexpression of selective OPN receptors and inflammatory response genes was enhanced in peripheral blood mononuclear cells from GD patients. Furthermore, serum from GD patients activated NF-κB activity in vitro, which was significantly suppressed by OPN monoclonal antibody abrogation. Conclusion: These data indicated a clinical correlation between serum OPN levels and GD. OPN could affect GD development through NF-κB activation and the subsequent changes in inflammatory milieu. OPN could serve as a novel biomarker for GD as well as a potential target for GD treatment.


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