TY - JOUR
T1 - Experimental autoimmune thyroiditis in human parvovirus B19 transgenic mice
AU - Mori, Kouki
AU - Yoshida, Katsumi
AU - Ishii, Keiko
AU - Morohoshi, Kazuki
AU - Nakagawa, Yoshinori
AU - Hoshikawa, Saeko
AU - Ozaki, Hiroshi
AU - Takahashi, Yurie
AU - Ito, Sadayoshi
N1 - Funding Information:
Declaration of interest: This study was presented in part at the 9th Asia and Oceania Thyroid Association Congress, Nagoya, Japan, November 2009, and was supported in part by grant-in-aid from Yamaguchi Endocrine Research Association. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
Copyright:
Copyright 2012 Elsevier B.V., All rights reserved.
PY - 2011/9
Y1 - 2011/9
N2 - Viral infection is implicated as a cause of autoimmune diseases. Whereas its role in Hashimoto's thyroiditis (HT) remains undefined, recent studies suggested a link between human parvovirus B19 (B19) infection and HT. We tested such possibility by using B19 nonstructural protein 1 (NS1) transgenic C57BL/6 mice, which harbor nonpermissive genetic background (H-2 b). Mice were immunized with either thyroglobulin (Tg) or saline. No thyroiditis developed in saline-treated mice and Tg-immunized males regardless of the presence or absence of NS1. In contrast, thyroiditis was induced by Tg immunization in 25% of transgenic females, but not in wild-type females. However, the thyroiditis incidence in the former did not differ significantly from that of the latter. In addition, intrathyroidal T-cell receptor gene expression was not augmented in Tg-immunized transgenic females. Immunization with Tg led to a comparable increase in serum anti-Tg antibody levels in the wild-type and transgenic mice. Our results indicate that the introduction of B19 NS1 gene into C57BL/6 mice is insufficient to promote the development of autoimmune thyroiditis. Further studies are required, however, before concluding that B19 infection is not involved in HT induction.
AB - Viral infection is implicated as a cause of autoimmune diseases. Whereas its role in Hashimoto's thyroiditis (HT) remains undefined, recent studies suggested a link between human parvovirus B19 (B19) infection and HT. We tested such possibility by using B19 nonstructural protein 1 (NS1) transgenic C57BL/6 mice, which harbor nonpermissive genetic background (H-2 b). Mice were immunized with either thyroglobulin (Tg) or saline. No thyroiditis developed in saline-treated mice and Tg-immunized males regardless of the presence or absence of NS1. In contrast, thyroiditis was induced by Tg immunization in 25% of transgenic females, but not in wild-type females. However, the thyroiditis incidence in the former did not differ significantly from that of the latter. In addition, intrathyroidal T-cell receptor gene expression was not augmented in Tg-immunized transgenic females. Immunization with Tg led to a comparable increase in serum anti-Tg antibody levels in the wild-type and transgenic mice. Our results indicate that the introduction of B19 NS1 gene into C57BL/6 mice is insufficient to promote the development of autoimmune thyroiditis. Further studies are required, however, before concluding that B19 infection is not involved in HT induction.
KW - Hashimoto's thyroiditis
KW - Human parvovirus B19
KW - Nonstructural protein 1
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U2 - 10.3109/08916934.2010.547891
DO - 10.3109/08916934.2010.547891
M3 - Article
C2 - 21332425
AN - SCOPUS:80051535558
VL - 44
SP - 483
EP - 489
JO - Autoimmunity
JF - Autoimmunity
SN - 0891-6934
IS - 6
ER -