@phdthesis{oai:nagasaki-u.repo.nii.ac.jp:00004868,
 author = {安井, 順一},
 month = {Mar},
 note = {We have previously shown that wild type (wt) mice exhibit susceptibility to immunization with human (h) thyrotropin receptor (TSHR), but resistance to mouse (m) TSHR, while TSHR knockout (KO) mice are susceptible to mTSHR, indicating the existence of robust immune tolerance against the mTSHR in wt mice. This tolerance may be mediated by either centrally or peripherally. We here explored the contribution of a peripheral arm of immune tolerance against the mTSHR by using antibodies to deplete regulatory T cells (Tregs), to antagonize co-inhibitory molecules and/or to stimulate co-stimulatory molecules. Antagonistic anti-co-inhibitory molecules, cytotoxic T lymphocyte antigen 4 (CTLA4) and programmed cell death 1 ligand 1 (PDL1), induced only low levels of anti-TSHR antibodies without induction of hyperthyroidism in a mouse Graves'model. In this experimental setting, antibody levels were significantly higher in THSR+/- mice than wt mice. However, agonistic anti-co-stimulatory molecules, CD40 and CD137, and Treg-depleting anti-CD25 antibodies showed no effect. All these data suggest that peripheral immune tolerance against the mTSHR may play a minor role, and imply the importance of central tolerance, in immune tolerance against mTSHR in mice. Additional studies on central tolerance to the mTSHR will be necessary for completely delineating the mechanisms for immune tolerance against mTSHR in mice., 長崎大学学位論文 学位記番号:博(医歯薬)甲第770号 学位授与年月日:平成27年3月20日, Author: Yasui Junichi, Nakahara Mami, Shimamura Mika, Kurashige Tomomi, Yasui Kazuaki, Abiru Norio, Kawakami Atsushi, Nagayama Yuji, Citation: Acta medica Nagasakiensia, 59(1), pp.13-17; 2014, Nagasaki University (長崎大学), 博士(医学) (2015-03-20)},
 school = {Nagasaki University (長崎大学)},
 title = {Minor contribution of cytotoxic T lymphocyte antigen 4 and programmed cell death ligand 1 in immune tolerance against mouse thyrotropin receptor in mice},
 year = {2015}
}