来自年轻非肥胖糖尿病（NOD）胰岛的CD8 T细胞克隆能够在没有CD4细胞的情况下，使NOD小鼠迅速发生糖尿病。
CD8 T cell clones from young nonobese diabetic (NOD) islets can transfer rapid onset of diabetes in NOD mice in the absence of CD4 cells.
作者信息
Wong F S, Visintin I, Wen L, Flavell R A, Janeway C A
机构信息
Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
出版信息
J Exp Med. 1996 Jan 1;183(1):67-76. doi: 10.1084/jem.183.1.67.
Abstract
T cells play an important role in the pathogenesis of diabetes in the nonobese diabetic (NOD) mouse. CD8 cytotoxic T cell lines and clones were generated from the lymphocytic infiltrate in the islets of Langerhans of young (7-wk-old). NOD mice by growing them on (NOD x B6-RIP-B7-1)F1 islets. These cells proliferate specifically to NOD islets and kill NOD islets in vitro. The cells are restricted by H-2Kd, and all bear T cell antigen receptor encoded by V beta 6. When these CD8 T cell lines and clones are adoptively transferred to irradiated female NOD, young NOD-SCID, and CB17-SCID mice, diabetes occurs very rapidly, within 10 d of transfer and without CD4 T cells.
摘要
T细胞在非肥胖糖尿病（NOD）小鼠糖尿病发病机制中起重要作用。从年轻（7周龄）NOD小鼠胰岛的淋巴细胞浸润中，通过在（NOD×B6-RIP-B7-1）F1胰岛上培养，产生了CD8细胞毒性T细胞系和克隆。这些细胞在体外可特异性增殖至NOD胰岛并杀伤NOD胰岛。这些细胞受H-2Kd限制，均携带由Vβ6编码的T细胞抗原受体。当将这些CD8 T细胞系和克隆过继转移至经辐照的雌性NOD、年轻NOD-SCID和CB17-SCID小鼠时，糖尿病在转移后10天内迅速发生，且无需CD4 T细胞。
相似文献
1
CD8 T cell clones from young nonobese diabetic (NOD) islets can transfer rapid onset of diabetes in NOD mice in the absence of CD4 cells.来自年轻非肥胖糖尿病（NOD）胰岛的CD8 T细胞克隆能够在没有CD4细胞的情况下，使NOD小鼠迅速发生糖尿病。
J Exp Med. 1996 Jan 1;183(1):67-76. doi: 10.1084/jem.183.1.67.
2
Major histocompatibility complex class I-restricted infiltration and destruction of pancreatic islets by NOD mouse-derived beta-cell cytotoxic CD8+ T-cell clones in vivo.在体内，NOD小鼠来源的β细胞细胞毒性CD8 + T细胞克隆对主要组织相容性复合体I类限制的胰岛浸润和破坏。
Diabetes. 1996 Aug;45(8):1121-31. doi: 10.2337/diab.45.8.1121.
3
The role of lymphocyte subsets in accelerated diabetes in nonobese diabetic-rat insulin promoter-B7-1 (NOD-RIP-B7-1) mice.淋巴细胞亚群在非肥胖糖尿病大鼠胰岛素启动子-B7-1（NOD-RIP-B7-1）小鼠加速糖尿病中的作用。
J Exp Med. 1998 Jun 15;187(12):1985-93. doi: 10.1084/jem.187.12.1985.
4
CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice.CD8细胞毒性T细胞克隆可迅速将自身免疫性糖尿病转移至非常年幼的非肥胖糖尿病（NOD）小鼠以及与MHC I类兼容的严重联合免疫缺陷（scid）小鼠体内。
Diabetologia. 1997 Sep;40(9):1044-52. doi: 10.1007/s001250050786.
5
Presentation of beta-cell antigens to CD4+ and CD8+ T cells of non-obese diabetic mice.向非肥胖糖尿病小鼠的CD4+和CD8+ T细胞呈递β细胞抗原。
J Immunol. 1993 Aug 1;151(3):1723-30.
6
Dysregulated B7-1 and B7-2 expression on nonobese diabetic mouse B cells is associated with increased T cell costimulation and the development of insulitis.非肥胖糖尿病小鼠B细胞上B7-1和B7-2表达失调与T细胞共刺激增加及胰岛炎的发展有关。
J Immunol. 2005 Jan 15;174(2):680-7. doi: 10.4049/jimmunol.174.2.680.
7
8
Evidence for the role of CD8+ cytotoxic T cells in the destruction of pancreatic beta-cells in nonobese diabetic mice.CD8 + 细胞毒性T细胞在非肥胖糖尿病小鼠胰腺β细胞破坏中作用的证据。
J Immunol. 1994 Feb 15;152(4):2042-50.
9
Transfer of diabetes in the NOD-scid mouse by CD4 T-cell clones. Differential requirement for CD8 T-cells.通过CD4 T细胞克隆将糖尿病转移至NOD-scid小鼠。对CD8 T细胞的不同需求。
Diabetes. 1996 Mar;45(3):328-36. doi: 10.2337/diab.45.3.328.
10
The influence of the major histocompatibility complex on development of autoimmune diabetes in RIP-B7.1 mice.主要组织相容性复合体对RIP-B7.1小鼠自身免疫性糖尿病发展的影响。
Diabetes. 2005 Jul;54(7):2032-40. doi: 10.2337/diabetes.54.7.2032.
引用本文的文献
1
Immunopeptidomics for autoimmunity: unlocking the chamber of immune secrets.自身免疫性疾病的免疫肽组学：开启免疫奥秘之室
NPJ Syst Biol Appl. 2025 Jan 17;11(1):10. doi: 10.1038/s41540-024-00482-x.
2
Immunomodulatory Functions of TNF-Related Apoptosis-Inducing Ligand in Type 1 Diabetes.肿瘤坏死因子相关凋亡诱导配体在 1 型糖尿病中的免疫调节功能。
Cells. 2024 Oct 10;13(20):1676. doi: 10.3390/cells13201676.
3
Cerebellar degeneration in gluten ataxia is linked to microglial activation.麸质共济失调中的小脑变性与小胶质细胞激活有关。
Brain Commun. 2024 Mar 7;6(2):fcae078. doi: 10.1093/braincomms/fcae078. eCollection 2024.
4
Insulin B-chain hybrid peptides are agonists for T cells reactive to insulin B:9-23 in autoimmune diabetes.胰岛素 B 链杂合肽是自身免疫性糖尿病中针对胰岛素 B:9-23 反应的 T 细胞的激动剂。
Front Immunol. 2022 Aug 10;13:926650. doi: 10.3389/fimmu.2022.926650. eCollection 2022.
5
A gut microbial peptide and molecular mimicry in the pathogenesis of type 1 diabetes.肠道微生物肽与 1 型糖尿病发病机制中的分子模拟现象。
Proc Natl Acad Sci U S A. 2022 Aug 2;119(31):e2120028119. doi: 10.1073/pnas.2120028119. Epub 2022 Jul 25.
6
Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.胰腺β细胞中半乳糖凝集素-3的转基因过表达减轻小鼠高血糖：与外源性白细胞介素-33的协同抗糖尿病作用
Front Pharmacol. 2021 Nov 5;12:714683. doi: 10.3389/fphar.2021.714683. eCollection 2021.
7
Toll-like receptor 7 deficiency suppresses type 1 diabetes development by modulating B-cell differentiation and function.Toll 样受体 7 缺陷通过调节 B 细胞分化和功能抑制 1 型糖尿病的发展。
Cell Mol Immunol. 2021 Feb;18(2):328-338. doi: 10.1038/s41423-020-00590-8. Epub 2021 Jan 11.
8
Identifying the 'Achilles heel' of type 1 diabetes.找出 1 型糖尿病的“阿喀琉斯之踵”。
Clin Exp Immunol. 2021 May;204(2):167-178. doi: 10.1111/cei.13570. Epub 2021 Feb 22.
9
Differentiating MHC-Dependent and -Independent Mechanisms of Lymph Node Stromal Cell Regulation of Proinsulin-Specific CD8 T Cells in Type 1 Diabetes.区分 MHC 依赖性和非依赖性机制在 1 型糖尿病中调节胰岛素原特异性 CD8 T 细胞的淋巴结基质细胞。
Diabetes. 2021 Feb;70(2):529-537. doi: 10.2337/db19-1050. Epub 2020 Oct 29.
10
Altered Systemic and Intestinal IgA Immune Responses in Individuals With Type 1 Diabetes.1 型糖尿病个体中系统性和肠道 IgA 免疫应答的改变。
J Clin Endocrinol Metab. 2020 Dec 1;105(12):e4616-25. doi: 10.1210/clinem/dgaa590.
本文引用的文献
1
Constructing polycompetitor cDNAs for quantitative PCR.构建用于定量PCR的多竞争型cDNA
J Immunol Methods. 1993 Sep 27;165(1):37-46. doi: 10.1016/0022-1759(93)90104-f.
2
The role of the CD28 receptor during T cell responses to antigen.CD28受体在T细胞对抗原反应过程中的作用。
Annu Rev Immunol. 1993;11:191-212. doi: 10.1146/annurev.iy.11.040193.001203.
3
Major histocompatibility complex class I-deficient NOD-B2mnull mice are diabetes and insulitis resistant.主要组织相容性复合体I类缺陷的NOD-B2m基因敲除小鼠对糖尿病和胰岛炎具有抗性。
Diabetes. 1994 Mar;43(3):505-9. doi: 10.2337/diab.43.3.505.
4
Beta 2-microglobulin-deficient NOD mice do not develop insulitis or diabetes.β2-微球蛋白缺陷的非肥胖糖尿病（NOD）小鼠不会发生胰岛炎或糖尿病。
Diabetes. 1994 Mar;43(3):500-4. doi: 10.2337/diab.43.3.500.
5
Major histocompatibility complex class I molecules are required for the development of insulitis in non-obese diabetic mice.主要组织相容性复合体I类分子是非肥胖糖尿病小鼠胰岛炎发展所必需的。
Eur J Immunol. 1993 Dec;23(12):3358-60. doi: 10.1002/eji.1830231244.
6
Mononuclear cell infiltration and its relation to the expression of major histocompatibility complex antigens and adhesion molecules in pancreas biopsy specimens from newly diagnosed insulin-dependent diabetes mellitus patients.新诊断的胰岛素依赖型糖尿病患者胰腺活检标本中的单核细胞浸润及其与主要组织相容性复合体抗原和黏附分子表达的关系。
J Clin Invest. 1993 Nov;92(5):2313-22. doi: 10.1172/JCI116835.
7
Presentation of beta-cell antigens to CD4+ and CD8+ T cells of non-obese diabetic mice.向非肥胖糖尿病小鼠的CD4+和CD8+ T细胞呈递β细胞抗原。
J Immunol. 1993 Aug 1;151(3):1723-30.
8
MHC-linked diabetogenic gene of the NOD mouse: molecular mapping of the 3' boundary of the diabetogenic region.非肥胖糖尿病（NOD）小鼠的主要组织相容性复合体（MHC）连锁致糖尿病基因：致糖尿病区域3'边界的分子定位
Biochem Biophys Res Commun. 1993 Apr 30;192(2):677-82. doi: 10.1006/bbrc.1993.1468.
9
Evidence for a preferential V beta usage by the T cells which adoptively transfer diabetes in NOD mice.在非肥胖糖尿病（NOD）小鼠中，过继转移糖尿病的T细胞优先使用Vβ的证据。
Eur J Immunol. 1993 Mar;23(3):727-33. doi: 10.1002/eji.1830230324.
10
Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors.将糖尿病移植到免疫缺陷的NOD-scid/scid小鼠体内。来自糖尿病与糖尿病前期NOD.NON-Thy-1a供体的CD4+和CD8+ T细胞的相对贡献。
Diabetes. 1993 Jan;42(1):44-55. doi: 10.2337/diab.42.1.44.
Zotero 插件