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H-2E(k) expression influences thyroiditis induction by the thyroglobulin peptide (2495-2511).

作者信息

Chronopoulou E, Carayanniotis G

机构信息

Department of Medicine, Memorial University of Newfoundland, St. John's, Canada.

出版信息

Immunogenetics. 1993;38(2):150-3. doi: 10.1007/BF00190903.

DOI:10.1007/BF00190903
PMID:7683308
Abstract
摘要

相似文献

1
H-2E(k) expression influences thyroiditis induction by the thyroglobulin peptide (2495-2511).H-2E(k)的表达会影响甲状腺球蛋白肽(2495-2511)诱导的甲状腺炎。
Immunogenetics. 1993;38(2):150-3. doi: 10.1007/BF00190903.
2
Distinct genetic pattern of mouse susceptibility to thyroiditis induced by a novel thyroglobulin peptide.小鼠对一种新型甲状腺球蛋白肽诱导的甲状腺炎易感性的独特遗传模式。
Immunogenetics. 1994;39(1):21-8. doi: 10.1007/BF00171793.
3
Fine epitope mapping within the pathogenic thyroglobulin peptide 2340-2359: minimal epitopes retaining antigenicity across various MHC haplotypes are not necessarily immunogenic.在致病性甲状腺球蛋白肽 2340-2359 内进行精细表位作图:保留针对各种 MHC 单倍型的抗原性的最小表位不一定具有免疫原性。
Immunology. 2012 Mar;135(3):245-53. doi: 10.1111/j.1365-2567.2011.03538.x.
4
Delineation of five thyroglobulin T cell epitopes with pathogenic potential in experimental autoimmune thyroiditis.实验性自身免疫性甲状腺炎中五个具有致病潜力的甲状腺球蛋白T细胞表位的描绘。
J Immunol. 2002 Nov 1;169(9):5332-7. doi: 10.4049/jimmunol.169.9.5332.
5
Experimental autoimmune thyroiditis (EAT) induced by the thyroglobulin peptide (2596-2608): influence of H-2 and non H-2 genes.甲状腺球蛋白肽(2596 - 2608)诱导的实验性自身免疫性甲状腺炎(EAT):H - 2和非H - 2基因的影响
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6
H2E-derived Ealpha52-68 peptide presented by H2Ab interferes with clonal deletion of autoreactive T cells in autoimmune thyroiditis.由H2Ab呈递的源自H2E的Ealpha52 - 68肽干扰自身免疫性甲状腺炎中自身反应性T细胞的克隆清除。
J Immunol. 2008 May 15;180(10):7039-46. doi: 10.4049/jimmunol.180.10.7039.
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Reactivity of anti-thyroid antibodies to thyroglobulin tryptic fragments: comparison of autoimmune and non-autoimmune thyroid diseases.抗甲状腺抗体对甲状腺球蛋白胰蛋白酶片段的反应性:自身免疫性和非自身免疫性甲状腺疾病的比较。
Braz J Med Biol Res. 1999 Apr;32(4):449-55. doi: 10.1590/s0100-879x1999000400012.
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Induction of experimental autoimmune thyroiditis by a 5-10 Kd peptidic fragment from porcine thyroglobulin.用猪甲状腺球蛋白的5-10 Kd肽段诱导实验性自身免疫性甲状腺炎
Acta Endocrinol Suppl (Copenh). 1987;281:104-6. doi: 10.1530/acta.0.114s104.
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Pathogenicity of a human thyroglobulin peptide (2340-2359) in mice with high or low genetic susceptibility to thyroiditis.一种人甲状腺球蛋白肽(2340 - 2359)对甲状腺炎遗传易感性高或低的小鼠的致病性。
Immunology. 2007 Nov;122(3):343-9. doi: 10.1111/j.1365-2567.2007.02645.x. Epub 2007 Jun 29.
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Shared thyroglobulin epitopes in autoimmune thyroiditis.
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引用本文的文献

1
A novel pathogenic peptide of thyroglobulin (2208-2227) induces autoreactive T-cell and B-cell responses in both high and low responder mouse strains.一种新型甲状腺球蛋白致病肽(2208-2227)在高应答和低应答两种小鼠品系中均可诱导自身反应性 T 细胞和 B 细胞应答。
Immunology. 2014 Jun;142(2):300-6. doi: 10.1111/imm.12254.
2
Thyroglobulin as autoantigen: structure-function relationships.作为自身抗原的甲状腺球蛋白:结构与功能的关系
Rev Endocr Metab Disord. 2000 Jan;1(1-2):69-77. doi: 10.1023/a:1010016520778.
3
Distinct genetic pattern of mouse susceptibility to thyroiditis induced by a novel thyroglobulin peptide.

本文引用的文献

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Breeding of a non-obese, diabetic strain of mice.一种非肥胖型糖尿病小鼠品系的培育。
Jikken Dobutsu. 1980 Jan;29(1):1-13. doi: 10.1538/expanim1978.29.1_1.
2
In vitro T-lymphocyte proliferative response to mouse thyroglobulin in experimental autoimmune thyroiditis.实验性自身免疫性甲状腺炎中体外T淋巴细胞对小鼠甲状腺球蛋白的增殖反应。
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H-2 gene products influence susceptibility of target thyroid gland to damage in experimental autoimmune thyroiditis.H-2基因产物影响实验性自身免疫性甲状腺炎中靶甲状腺对损伤的易感性。
小鼠对一种新型甲状腺球蛋白肽诱导的甲状腺炎易感性的独特遗传模式。
Immunogenetics. 1994;39(1):21-8. doi: 10.1007/BF00171793.
4
Mapping of thyroglobulin epitopes: presentation of a 9mer pathogenic peptide by different mouse MHC class II isotypes.甲状腺球蛋白表位的定位:不同小鼠MHC II类同种型对一种9聚体致病肽的呈递
Immunogenetics. 1994;40(5):352-9. doi: 10.1007/BF01246676.
5
Autoreactive IgG elicited in mice by the non-dominant but pathogenic thyroglobulin peptide (2495-2511): implications for thyroid autoimmunity.由非优势但具有致病性的甲状腺球蛋白肽(2495 - 2511)在小鼠中引发的自身反应性IgG:对甲状腺自身免疫的影响。
Clin Exp Immunol. 1994 Oct;98(1):89-94. doi: 10.1111/j.1365-2249.1994.tb06612.x.
Eur J Immunol. 1980 Feb;10(2):156-9. doi: 10.1002/eji.1830100216.
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Syngeneic sensitization of mouse lymphocytes on monolayers of thyroid epithelial cells. IV. Correlation with H-2 haplotypes.
Cell Immunol. 1983 Jun;78(2):387-91. doi: 10.1016/0008-8749(83)90294-0.
5
Regulation of experimental autoimmune thyroiditis: influence of non-H-2 genes.实验性自身免疫性甲状腺炎的调控:非H-2基因的影响
J Immunogenet. 1982 Aug;9(4):257-65. doi: 10.1111/j.1744-313x.1982.tb00981.x.
6
Regulation of experimental autoimmune thyroiditis: mapping of susceptibility to the I-A subregion of the mouse H-2.实验性自身免疫性甲状腺炎的调控:小鼠H-2 I-A亚区易感性图谱
Immunogenetics. 1982;15(4):427-30. doi: 10.1007/BF00364266.
7
Selection of H-2 molecules for the context of antigen recognition by T lymphocytes.T淋巴细胞识别抗原背景下H-2分子的选择。
Immunogenetics. 1981;14(3-4):283-92. doi: 10.1007/BF00342197.
8
H-2K mutation controls immune response phenotype of autoimmune thyroiditis. Critical expression of mutant gene product in both thymus and thyroid glands.H-2K突变控制自身免疫性甲状腺炎的免疫反应表型。突变基因产物在胸腺和甲状腺中均有关键表达。
J Exp Med. 1980 Oct 1;152(4):1115-20. doi: 10.1084/jem.152.4.1115.
9
Syngeneic sensitization of mouse lymphocytes on monolayers of thyroid epithelial cells. V. The primary syngeneic sensitization is under I-A subregion control.小鼠淋巴细胞在甲状腺上皮细胞单层上的同基因致敏。V. 初次同基因致敏受I-A亚区控制。
Eur J Immunol. 1983 Nov;13(11):948-51. doi: 10.1002/eji.1830131115.
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Role of the Ek molecule in the generation of suppressor T cells in response to LDHB.Ek分子在响应LDHB产生抑制性T细胞过程中的作用。
Scand J Immunol. 1982 Jul;16(1):25-31. doi: 10.1111/j.1365-3083.1982.tb00695.x.