Evidence that MHC I-E dampens thyroid autoantibodies and prevents spreading to a second thyroid autoantigen in I-A(k) NOD mice.
Evidence that MHC I-E dampens thyroid autoantibodies and prevents spreading to a second thyroid autoantigen in I-A(k) NOD mice.
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作者：
点头。H2k和NOD。H2h4小鼠携带与实验诱导的甲状腺炎易感性相关的MHC II类分子I-Ak。膳食碘增强自发性甲状腺自身免疫，这在NOD中是众所周知的。H2h4小鼠，未在NOD中进行研究。H2k老鼠。我们比较了NOD。H2h4和NOD。H2k检测甲状腺炎和甲状腺球蛋白（TgAb）和甲状腺过氧化物酶（TPOAb）自身抗体，不加或加碘化钠（NaI）治疗32周。NOD患者TgAb水平明显升高。H2h4比NOD。NaI和TPOAb作用的H2k小鼠在NOD中发育。H2h4但不是NOD。H2k老鼠。DNA外显子组分析显示，除了染色体（Chr） 17 MHC区域的差异外，NOD。H2k，尤其是NOD。H2h4小鼠具有大量的非mhc亲本DNA。KEGG通路分析强调了Chr 17上的甲状腺自身免疫和免疫应答基因，而不是Chr 7和15亲本B10。A4R DNA。亲本菌株的研究没有提供非mhc基因贡献的证据。与实验诱导的甲状腺炎相关的外显子10甲状腺球蛋白单倍型在NOD中缺失。H2h4和NOD。H2k小鼠并不是自发性小鼠甲状腺自身免疫的标志。总之，I-E的缺失可能是NOD之间差异的一个解释。H2h4和NOD。H2k小鼠的TgAb水平和人类一样，自身抗体向TPO扩散。
NOD.H2k and NOD.H2h4 mice carry the MHC class II molecule I-Ak associated with susceptibility to experimentally-induced thyroiditis. Dietary iodine enhanced spontaneous thyroid autoimmunity, well known in NOD.H2h4 mice, has not been investigated in NOD.H2k mice. We compared NOD.H2h4 and NOD.H2k strains for thyroiditis and autoantibodies to thyroglobulin (TgAb) and thyroid peroxidase (TPOAb) without or with dietary sodium iodide (NaI) for up to 32 weeks. TgAb levels were significantly higher in NOD.H2h4 than NOD.H2k mice on NaI and TPOAb developed in NOD.H2h4 but not NOD.H2k mice. DNA exome analysis revealed, in addition to the differences in the chromosome (Chr) 17 MHC regions, that NOD.H2k and particularly NOD.H2h4 mice have substantial non-MHC parental DNA. KEGG pathway-analysis highlighted thyroid autoimmunity and immune-response genes on Chr 17 but not on Chr 7 and 15 parental B10.A4R DNA. Studies of parental strains provided no evidence for non-MHC gene contributions. The exon 10 thyroglobulin haplotype, associated with experimentally-induced thyroiditis, is absent in NOD.H2h4 and NOD.H2k mice and is not a marker for spontaneous murine thyroid autoimmunity. In conclusion, the absence of I-E is a likely explanation for the difference between NOD.H2h4 and NOD.H2k mice in TgAb levels and, as in humans, autoantibody spreading to TPO.
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DOI：
10.1084/jem.178.3.793
发表时间：
1993-09-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Podolin PL;Pressey A;DeLarato NH;Fischer PA;Peterson LB;Wicker LS
通讯作者：
Wicker LS
影响因子：
3.6
作者：
Ni, Peggy P.;Wang, Yaming;Allen, Paul M.
通讯作者：
Allen, Paul M.
影响因子：
64.8
作者：
NISHIMOTO, H;KIKUTANI, H;KISHIMOTO, T
通讯作者：
KISHIMOTO, T
影响因子：
4.3
作者：
Hutchings, PR;Verma, S;Cooke, A
通讯作者：
Cooke, A
影响因子：
4.3
作者：
Hillhouse, Erin E.;Collin, Roxanne;Lesage, Sylvie
通讯作者：
Lesage, Sylvie