Studies on thyroid autoimmunity: anti-TSHR immune response and tolerance in mice
| Project/Area Number |
24591368
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Endocrinology
|
|---|
| Research Institution | Nagasaki University |
|---|
Principal Investigator |
NAGAYAMA Yuji 長崎大学, 原爆後障害医療研究所, 教授 (30274632)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | バセドウ病 / マウスモデル / TSH受容体 / 国際情報交換：ドイツ：アメリカ / 国際情報交換、ドイツ |
|---|
| Outline of Final Research Achievements |
We have recently shown that (i) wt mice are tolerant, while TSHR KO mice are responsive to the mouse receptor in a mouse model of Graves’ disease using adenovirus expressing mouse TSHR, and (ii) anti-TSHR immune response could be adoptively transferred from TSHR KO to nude mice but that hyperthyroidism and TSAb were transient and soon changed to hypothyroidism and TBAb. Therefore, we here studied (i) the mechanisms of immune tolerance and response in wt KO mice, respectively, and (ii) those of immune response in the adoptive transfer model. In the evaluation of the peripheral tolerance, inhibition of co-inhibitory molecules and stimulation of co-stimulatory molecules increased the anti-TSHR antibodies, but did not develop TSAb or hyperthyroidism. On the other hand, the studies on central tolerance did not technically work well. In the adoptive transfer model, Graves’ disease could be maintained by repetitive immunization following transfer.
|
Report
(4 results)
Research Products
(22 results)
-
-
-
-
-
-
-
[Journal Article] Thyrotropin signaling confers more aggressive features with higher genomic instability on BRAFV600E-induced thyroid tumors in a mouse model.2014
Author(s)
Orim F, Bychkov A, Shimamura M, Nakashima M, Ito M, Matsuse M, Kurashige T, Suzuki K, Saenko V, Nagayama Y, Yamashita S, Mitsutake N
-
Journal Title
Thyroid
Volume: 24(3)
Issue: 3
Pages: 502-510
DOI
NAID
Related Report
Peer Reviewed
-
-
[Journal Article] Postnatal expression of BRAFV600E does not induce thyroid cancer in mouse models of thyroid papillary carcinoma2013
Author(s)
Shimamura M, Nakahara M, Orim F, Kurashige T, Mitsutake N, Nakashima M, Kondo S, Yamada M, Taguchi R, Kimura S, Nagayama Y
-
Journal Title
Endocrinology
Volume: 154
Issue: 11
Pages: 4423-30
DOI
NAID
Related Report
Peer Reviewed
-
-
[Journal Article] Genetic deletion of Granzyme B does not confer resistance to the development of spontaneous diabetes in NOD mice.2013
Author(s)
Kobayashi M, Kaneko-koike C, Abiru N, Uchida T, Akazawa S, Nakamura K, Kuriya G, Satoh T, Ida H, Kawasaki E, Yamasaki H, Nagayama Y, Sasak H, Kawakami A.
-
Journal Title
Clin Exp Immunol
Volume: in press
Related Report
Peer Reviewed
-
[Journal Article] Identification of new Cockayne syndrome patients deficient in the ERCC1 and XPF/ERCC4 gene.2013
Author(s)
Kashiyama K, Nakazawa Y, Shimada M, Sasaki K, Takahashi Y, Fawxett H, Lewin SO, Carr L, Yoshida K, Utani A, Hirano A, Yamashita S, Nagayama Y, Mitsutake N, Lehmann AR, Ogi T.
-
Journal Title
Am J Hum Gnenet
Volume: なし
Related Report
Peer Reviewed
-
[Journal Article] Double deficiency in IL-17 and IFN-g signaling significantly suppresses the development of diabetes in the NOD mouse.2013
Author(s)
Kuriya G, Abiru N, Kobayashi M, Nagayama Y, Akazawa S, Nakamura K, Sato T, Horie I, Kuwahara H, Kawasaki E, Yamasaki H, Yu L, Eisenbarth GS, Iwakura Y, Eguchi K.
-
Journal Title
Diabetologia
Volume: in press
Related Report
Peer Reviewed
-
-
-
-
-
-
-
-
-
