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Open access

Kusum Lata, Pinaki Dutta, Subbiah Sridhar, Minakshi Rohilla, Anand Srinivasan, G R V Prashad, Viral N Shah, and Anil Bhansali

effect on granulosa cells, luteal cells and oocyte maturation (8) . Euthyroid women with thyroid autoimmunity are twice as likely to experience spontaneous miscarriages (9) . This probably represents a generalised activation of the immune system, or an

Open access

Aaron Lerner, Patricia Jeremias, and Torsten Matthias

mucosa and luminal ecosystems involvement in the thyroid autoimmunity: (i) Gut dysbiosis might disturb the finely tuned immune balance and break tolerance to self-antigens and non-pathogenic non-self-antigens, by posttranslational modification proteins

Open access

Nancy J Olsen, Ann L Benko, and William J Kovacs

modulate autoimmunity. An association of Klinefelter's syndrome with lupus has been reported in several studies, and in isolated case reports, reversal of hypogonadism in such patients with Klinefelter's syndrome by testosterone replacement has been

Open access

Stavroula A Paschou, Nektaria Papadopoulou-Marketou, George P Chrousos, and Christina Kanaka-Gantenbein

pancreas. A small percentage of affected patients (<10%) are classified as type 1B, with no evidence of autoimmunity and the pathogenesis in these cases is considered idiopathic ( 1 , 2 ). The aim of this comprehensive review is to present updated

Open access

Borros Arneth


The origin of autoimmune disease type 1 diabetes is still unknown.


This study assessed the activation of CD4+ and CD8+ T-lymphocytes by human insulin and human glutamate decarboxylase (GAD) in patients with type 1 or type 2 diabetes mellitus (DM) and healthy volunteers.

Materials and methods

The expression of CD69, a marker of T-lymphocyte activity, was determined in whole blood samples by flow cytometry after 12 h of incubation with or without insulin or GAD. The analysis included samples from 12 type 1 DM patients, 14 type 2 DM patients and 12 healthy volunteers.


Significant increases in the number of activated CD4+ and CD8+ T-lymphocytes following pre-incubation of whole blood samples with human insulin or GAD were observed in samples from patients with type 1 DM, whereas no activation of these cells was detected in samples from either type 2 DM patients or healthy subjects.


These results indicated that latent pre-activation of CD4+ and CD8+ T-lymphocytes in response to insulin or GAD epitopes occurred in type 1 DM patients.


These findings suggest that pre-immunization against insulin and/or GAD might be associated with the development of type 1 DM. Alternatively, these results might reflect a non-specific, bystander autoimmune response.

Open access

Xiangyu Gao, Wanwan Sun, Yi Wang, Yawen Zhang, Rumei Li, Jinya Huang, and Yehong Yang

). Historically, based on positivity of islet autoantibodies, diabetes mellitus had been classified into two clinical types: type 1 diabetes (T1DM) and type 2 diabetes (T2DM) ( 3 , 4 ). The progressive destruction of islet β cell mass caused by islet autoimmunity

Open access

Qinglei Yin, Zhou Jin, Yulin Zhou, Dalong Song, Chenyang Fu, FengJiao Huang, and Shu Wang

of autoimmunity- and inflammation-related processes, including nuclear factor-κB and toll-like receptor signaling, cytokine expression, and immune cell proliferation and differentiation ( 15 , 16 , 17 , 18 , 19 ). It has also been demonstrated

Open access

Lauren Bell, Ann Louise Hunter, Angelos Kyriacou, Annice Mukherjee, and Akheel A Syed

compared to TRAb measurement in a UK university teaching hospital. Whereas previous observational studies involving thyroid autoimmunity in clinical practice have evaluated the sensitivity and specificity of TRAb tests against the premise of definitiveness

Open access

Emmi Naskali, Katja Dettmer, Peter J Oefner, Pedro A B Pereira, Kai Krohn, Petri Auvinen, Annamari Ranki, and Nicolas Kluger

ja Addison Ry, . Most of these patients have been included in various publications on APECED in Finland ( 1 , 13 ), including our previous work about gastrointestinal autoimmunity ( 9 ). The mean age of the cohort was 39

Open access

Stine Linding Andersen and Stig Andersen

The management of hyperthyroidism in pregnant patients has been a topic of raised clinical awareness for decades. It is a strong recommendation that overt hyperthyroidism of Graves’ disease in pregnant women should be treated to prevent complications. The consequences of hyperthyroidism in pregnancy are less studied than hypothyroidism, and a literature review illustrates that the main burden of evidence to support current clinical guidance emerges from early observations of severe complications in Graves’ disease patients suffering from untreated hyperthyroidism in the pregnancy. On the other hand, the more long-term consequences in children born to mothers with hyperthyroidism are less clear. A hypothesis of fetal programming by maternal hyperthyroidism implies that excessive levels of maternal thyroid hormones impair fetal growth and development. Evidence from experimental studies provides clues on such mechanisms and report adverse developmental abnormalities in the fetal brain and other organs. Only few human studies addressed developmental outcomes in children born to mothers with hyperthyroidism and did not consistently support an association. In contrast, large observational human studies performed within the last decade substantiate a risk of teratogenic side effects to the use of antithyroid drugs in early pregnancy. Thus, scientific and clinical practice are challenged by the distinct role of the various exposures associated with Graves’ disease including the hyperthyroidism per se, the treatment, and thyroid autoimmunity. More basic and clinical studies are needed to extend knowledge on the effects of each exposure, on the potential interaction between exposures and with other determinants, and on the underlying mechanisms.