|
|
||||||||
Letters |
1 Department of Biomedical Informatics, Division of Health Sciences, Osaka University Graduate School of Medicine, Osaka, Japan
2 Translational Research Center, Kyoto University Hospital, Kyoto University School of Medicine, Kyoto, Japan
aAddress correspondence to this author at: Department of Biomedical Informatics Division of Health Sciences, Osaka University Graduate School of Medicine, 1-7 Yamadaoka, Suita, Osaka 565-0871, Japan, Fax 81-6-6879-2592 e-mail iwatani@sahs.med.osaka-u.ac.jp
| The first 20% of the full text of this article appears below. |
To the Editor:
The severity of Hashimoto disease (HD) varies among patients and is difficult to predict when the disease is in the subclinical state and diagnosed by the presence of thyroid-specific autoantibody. Likewise, the intractability of Graves disease (GD) is difficult to predict. Autoimmune thyroid destruction that underlies both diseases is strongly determined by T-cell cytotoxicity, which is activated by interferon (IFN)-
(1), and the T allele in +874A/T polymorphism of the interferon gamma (IFNG) gene, which promotes increased IFN-
production, has been noted more frequently among patients with severe HD (2). Cytokine balance between T-helper 1 (Th1) cytokines, such as IFN-
, and Th2 cytokines is important in immune regulation (3). Therefore, it is possible that Th2 cytokines may also affect the severity of
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |