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Immune Renal Injury: Similarities and Differences Between Glomerular Diseases and Transplantation

-1659. 4. Land W. Innate autoimmunity: history and current knowledge. Clin Transplant 2007; 5: 575-584. 5. Debiec H, Guigonis V, Mougenot B, et al . Antenatal membranous glomerulonephritis due to neutral endopeptidase antibodies. N Engl J Med 2002; 346: 2053-2060. 6. Beck LH Jr, Bonegio RG, Lambeau G, et al . M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med 2009; 361: 11-21. 7. Puttarajappa C, Shapiro R, Henkie P. Antibody-Mediated Rejection in Kidney Transplantation: A Review. J Transplant

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Role of interlekin-35 as a biomarker in patients with newly diagnosed Hashimoto’s thyroiditis

, Castellaw AH, Lennon GP, Burton AR, Vignali DA. Prevention of autoimmune diabetes by ectopic pancreatic β-cell expression of interleukin-35. Diabetes 61, 1519-1526, 2012. Bossowski A, Moniuszko M, Dąbrowska M, Sawicka B, Rusak M, Jeznach M, Wojtowicz J, Bodzenta-Lukaszyk A, Bossowska A. Lower proportions of CD4+CD25(high) and CD4+FoxP3, but not CD4+CD25+CD127(low) FoxP3+ T cell levels in children with autoimmune thyroid diseases. Autoimmunity 46, 222-230, 2013. Caturegli P, De Remigis A, Rose NR. Hashimoto thyroiditis: clinical and

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Vitamin D and thyroid autoimmunity

-88; 4. Kamen, D.L., Cooper, G.S., Bouali, H., Shaftman, S.R., Hollis, B.W. &Gilkeson, G.S. (2006). Vitamin D deficiency in systemic lupus erythematosus. Autoimmun Rev. 5,114-117. doi:10.1016/j.autrev.2005.05.009. 5. Runia, T.F., Hop, W.C., De Rijke, Y.B., Buljevak D. & Hintzen, R.Q. (2012). Lower serum vitamin D levels are associated with a higher relapse risk in multiple sclerosis. Neurology.(79), 261-266. 6. Varenna, M., Manara, M., Cantatore, F. P., Del Puente, A., Di Munno, O., Malavolta, N., Minisola, G., Adami, S., Sinigaglia, L

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Pathogenesis of Type 1 Diabetes Mellitus: A Brief Overview

References Karlsen AE, Sparre T, Nielsen K, Nerup J, Pociot F. Proteome analysis - a novel approach to understand the pathogenesis of type 1 diabetes mellitus. Dis Markers 17: 205-216, 2001. Redondo MJ, Rewers M, Yu L, Garg S, Pilcher CC, Elliott RB, Eisenbarth GS. Genetic determination of islet cell autoimmunity in monozygotic twin, dizygotic twin, and non-twin siblings of patients with type 1 diabetes: prospective twin study. BMJ 318: 698-702, 1999. Karavanaki K, Tsoka E

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Regarding the trigger of the beta cell autoimmunity

on etiology. J Autoimmun doi: 10.1016/j.jaut.2013.10.001, 2013. [Epub ahead of print] 18. Erlich HA, Valdes AM, Noble JA. Prediction of type 1 diabetes. Diabetes 62: 1020-1021, 2013. 19. Todd JA. Etiology of type 1 diabetes. Immunity 32: 457-467, 2010. 20. Ionescu-Tirgoviste C, Gagniuc P, Guja C. The promoters of genes associated with type 1 and type 2 diabetes seem to have some specific features. Diabetologia 55[Suppl1]: S123, 2012. (Abstract 280) 21. Cnop M, Hughes SJ, Igoillo-Esteve M et al. The

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Clinical, Genetic and Immunological Characteristics of Paediatric Autoimmune Polyglandular Syndrome Type 1 Patients in Slovenia / Klinične, Genetske nn Imunološke Značilnosti Otrok In Mladostnikov Z Avtoimunskim Poliglandularnim Sindromom Tipa 1 V Sloveniji

M. et al. Positional cloning of the APECED gene. Nat Genet 1997; 17: 393-8. 4. Liston A, Lasage S, Wilson J, Peltonen L, Goodnow CC. Aire regulates negative selection of organ-specific T-cells. Nat Immunol 2003; 4: 350-4. 5. Peterson P, Peltonen L. Autoimmune polyglandular syndrome type 1 (APS1) and AIRE gene: new views on molecular basis od autoimmunity. J Autoimmun 2005; 25: 49-55. 6. Meager A, Visvalingam K, Peterson P, Möll K, Murumägi A, Krohn K. et al. Anti-interferon autoantibodies in autoimmune

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Monocytes/Macrophages Act as Mediators for Human Herpesvirus-6 Infection of Thyroid Gland in Patients with Autoimmune Thyroiditis

Abstract

The aim of this study was to investigate the possibility of using monocytes/macrophages as mediators in human herpesvirus-6 (HHV-6) infection of thyroid gland tissues in autoimmune thyroiditis (AIT). Seventy-three AIT patients were enrolled in this study. The control group consisted of 80 blood donors. Monocyte/macrophage isolation for AIT patient samples was performed by adherence. HHV-6 was detected in peripheral blood mononuclear cell (PBMC) DNA samples using nested polymerase chain reaction (nPCR). Gene expression of HHV-6 active infection marker (U79/80) and chemokine receptors (U12, U51) in patient monocyte/macrophage samples and blood donor PBMC samples was detected using reverse-transcription PCR. HHV-6 viral load was detected by using quantitative-PCR technique. The HHV-6 genomic sequence was found significantly more frequently among AIT patient than control group samples. Markers of active infection were found in 8 AIT patient monocyte/macrophage samples (11%) and in none of control group PBMC samples. HHV-6 U51 mRNA expression was detected only in AIT patient samples (2/24 previously positive for HHV-6). Since HHV-6 genomic sequences were found significantly more frequently in AIT patient samples and active infection markers were found in patient monocytes/macrophages, our results suggest that monocytes/macrophages may be used by HHV-6 as mediators for thyroid gland infection.

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Possible Involvement of Human Herpesvirus-6 U83 Gene Expression in Autoimmune Thyroiditis Development

Abstract

Viral infections have been frequently cited as important environmental factors implicated in autoimmune thyroiditis (AIT) development, although no specific virus has yet been conclusively associated with the disease. Some evidence implicates human herpesvirus-6 (HHV-6) in this disease. The aim of this study was to investigate the role of the HHV-6 U83 gene expression in autoimmune thyroiditis development. Fifty-one patients with AIT following thyroidectomy and a control group of 30 autopsied subjects without thyroid pathologies for comparing virology results and 30 healthy blood donors for comparing serology results were enrolled in this study. HHV-6 U83 gene expression was determined using nested PCR with complementary DNA as the template acquired from thyroid gland extracted RNA. Plasma samples of AIT patients and blood donors were tested for IL-2, IL-4, IL-10, sTNF-RII and IL-1beta levels by ELISA. Virology results were compared with pro- and anti-inflammatory cytokine levels to determine possible interaction of HHV-6 with host immune response. HHV-6 U83 gene expression was found only in 24% (12/49) of AIT patient thyroid gland tissue samples and in none of the control group individuals, showing possible involvement of this gene in AIT development. However, no interaction between HHV-6 and changes in cytokine levels was found.

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Thyroid screening in pregnancy - a compulsory preventive activity

ABSTRACT

Obiectives: To assess the prevalence of thyroid dysfunction in a group of pregnant women, originating from Dobrogea region of southeastern Romania, considered to be an area without iodine deficiency, including the Black Sea area. Materials and methods: We enrolled 324 pregnant women in different trimesters of pregnancy. Each case was reviewed by a detailed madical history, clinical examination and by serum dosage of thyroid hormones: TSH, FT4, and the antithyroidperoxidase. They were evaluated by comparison with trimester -specific reference range for TSH recommended by American Thyroid Association, then the results were compared with those obtained using the manufacturers reference range. Abortion rate was also analysed. Results: The prevalence of thyroid dysfunction was different in all the 3 trimesters: subclinical hypothyroidism being the most frequently approx. 24% of all cases; 7% of pregnant women had overt hypothyroidism. Incidence of thyrotoxicosis in entire study cases was approx. 5.5%. The most frecvent thyroid autoimune disorders were Hashimoto thyroiditis: 42 % - I trimester, 26,6% in II trimester and about 12,5 % in III-trimester; Graves disease have an incidence of only 0,9 % (n=3).The difference between reference methods eluded a lower number of cases using manufactures reference range for TSH (P< 0,001), but higher for recommended trimester - specific TSH value, confirming the undervalueted hypothesis. The risk of misclassifying the hypothyroidism is between 3 %-8 %. Conclusion: Necessity for thyroid hormone dosage periodic/trimesterly/ in pregnancy is a preventive measure. The reference values for hormonal dosage requires trimester-specific assessment. The possibility of hormonal disorders during pregnancy is common. The need for specific therapy at diagnosis depends on the nature of hormonal disorder. Further precautions are needed in pregnant women with known autoimmune thyroid disorder or newly diagnosed

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