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NZB小鼠中耐受性诱导缺陷的研究。骨髓前T细胞缺陷的证据。

Studies of defective tolerance induction in NZB mice. Evidence for a marrow pre-T cell defect.

作者信息

Laskin C A, Smathers P A, Reeves J P, Steinberg A D

出版信息

J Exp Med. 1982 Apr 1;155(4):1025-36. doi: 10.1084/jem.155.4.1025.

DOI:10.1084/jem.155.4.1025
PMID:6977614
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2186644/
Abstract

NZB mice manifest a defect in tolerance induction by deaggregated heterologous gamma globulins. We have used an adoptive transfer system to study the defect. Thymectomized, intact, or thymectomized recipients given thymic epithelial grafts were studied after lethal irradiation and reconstitution with NZB, DBA/2, or (NZB x DBA(F1 marrow depleted of mature T cells. NZB thymocytes were responsible for the tolerance defect of NZB mice. The information for the defect was present in the NZB marrow prethymocyte. That defect could only be expressed when there was further maturation in association with a thymus. However, the normal DBA/2 thymic epithelium served as well as the abnormal NZB thymic epithelium. These studies resolve existing conflicts as to whether the NZB marrow or thymus is responsible for the loss of tolerance in association with autoimmunity.

摘要

新西兰黑鼠（NZB）在通过解聚的异源γ球蛋白诱导耐受性方面表现出缺陷。我们采用了一种过继转移系统来研究该缺陷。对经致死性照射并用去除成熟T细胞的NZB、DBA/2或（NZB×DBA）F1骨髓进行重建后的去胸腺、完整或接受胸腺上皮移植的受体进行了研究。NZB胸腺细胞导致了NZB小鼠的耐受性缺陷。该缺陷的信息存在于NZB骨髓前体细胞中。只有在与胸腺相关的进一步成熟过程中，该缺陷才能表达。然而，正常的DBA/2胸腺上皮与异常的NZB胸腺上皮发挥的作用相同。这些研究解决了关于NZB骨髓或胸腺是否与自身免疫相关的耐受性丧失有关的现有争议。

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Studies of defective tolerance induction in NZB mice. Evidence for a marrow pre-T cell defect.NZB小鼠中耐受性诱导缺陷的研究。骨髓前T细胞缺陷的证据。
J Exp Med. 1982 Apr 1;155(4):1025-36. doi: 10.1084/jem.155.4.1025.
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本文引用的文献

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The cellular and genetic basis of murine lupus.小鼠狼疮的细胞和遗传基础。
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H-2 restriction as a consequence of intentional priming. Frequency analysis of alloantigen-restricted, trinitrophenyl-specific cytotoxic T lymphocyte precursors within thymocytes of normal mice.作为有意致敏结果的H-2限制。正常小鼠胸腺细胞内同种抗原限制的、三硝基苯基特异性细胞毒性T淋巴细胞前体的频率分析。
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3
Evidence for abnormalities in separate lymphocyte populations in NZB mice.新西兰黑鼠（NZB）中不同淋巴细胞群体异常的证据。
J Immunol. 1980 Aug;125(2):485-90.
4
Gene complementation. Neither Ir-GLphi gene need be present in the proliferative T cell to generate an immune response to Poly(Glu55Lys36Phe9)n.基因互补。在增殖性T细胞中，无需存在任何一个Ir - GLphi基因即可对聚（Glu55Lys36Phe9）n产生免疫反应。
J Exp Med. 1980 Jun 1;151(6):1452-67. doi: 10.1084/jem.151.6.1452.
5
Immunoregulatory circuits that modulate responsiveness to suppressor cell signal. Failure of B10 mice to respond to suppressor factors can be overcome by quenching the contrasuppressor circuit.调节对抑制性细胞信号反应性的免疫调节回路。通过消除反抑制回路可克服B10小鼠对抑制因子无反应的情况。
J Exp Med. 1981 Jun 1;153(6):1547-61. doi: 10.1084/jem.153.6.1547.
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Contrasuppression. A novel immunoregulatory activity.反向抑制。一种新型免疫调节活性。
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7
T cell abnormalities in NZB mice occur independently of autoantibody production.NZB小鼠的T细胞异常独立于自身抗体产生而发生。
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J Exp Med. 1980 Sep 1;152(3):748-53. doi: 10.1084/jem.152.3.748.
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Frequency analysis of cytotoxic T lymphocyte precursors in chimeric mice. Evidence for intrathymic maturation of clonally distinct self-major histocompatibility complex- and allo-major histocompatiblilty complex-restricted virus-specific T cells.嵌合小鼠中细胞毒性T淋巴细胞前体的频率分析。克隆性不同的自身主要组织相容性复合体和同种异体主要组织相容性复合体限制性病毒特异性T细胞胸腺内成熟的证据。
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