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1
A new T cell subset expressing B220 and CD4 in lpr mice: defects in the response to mitogens and in the production of IL-2.lpr小鼠中表达B220和CD4的新型T细胞亚群：对丝裂原反应及白细胞介素-2产生存在缺陷
Clin Exp Immunol. 1988 Oct;74(1):36-40.
2
Evidence for early onset, polyclonal activation of T cell subsets in mice homozygous for lpr.在纯合 lpr 基因的小鼠中 T 细胞亚群早期发作、多克隆激活的证据。
J Immunol. 1992 Nov 1;149(9):3097-106.
3
Evidence for the existence of two parallel differentiation pathways in the thymus of MRL lpr/lpr mice.MRL lpr/lpr小鼠胸腺中两条平行分化途径存在的证据。
J Immunol. 1992 Aug 1;149(3):1069-74.
4
In CD8+ T cell-deficient lpr/lpr mice, CD4+B220+ and CD4+B220- T cells replace B220+ double-negative T cells as the predominant populations in enlarged lymph nodes.在CD8 + T细胞缺陷的lpr/lpr小鼠中，CD4 + B220 +和CD4 + B220 - T细胞取代B220 +双阴性T细胞，成为肿大淋巴结中的主要细胞群体。
J Immunol. 1995 May 15;154(10):4986-95.
5
CD2-CD4-CD8- lymph node T lymphocytes in MRL lpr/lpr mice are derived from a CD2+CD4+CD8+ thymic precursor.MRL lpr/lpr小鼠中CD2-CD4-CD8-淋巴结T淋巴细胞来源于CD2+CD4+CD8+胸腺前体细胞。
J Immunol. 1993 Jul 15;151(2):1086-96.
6
Dissociation of severe lupus-like disease from polyclonal B cell activation and IL 2 deficiency in C3H-lpr/lpr mice.C3H-lpr/lpr小鼠中严重狼疮样疾病与多克隆B细胞激活及白细胞介素2缺乏的解离
J Immunol. 1984 Aug;133(2):1048-56.
7
Functionally anergic lpr and gld B220+ T cell receptor (TCR)-alpha/beta+ double-negative T cells express CD28 and respond to costimulation with phorbol myristate acetate and antibodies to CD28 and the TCR.功能失能的lpr和gld B220+ T细胞受体（TCR）α/β+双阴性T细胞表达CD28，并对佛波醇肉豆蔻酸酯乙酸盐以及抗CD28和TCR的抗体的共刺激产生反应。
J Immunol. 1993 Jul 15;151(2):597-609.
8
Origin of CD4-CD8-B220+ T cells in MRL-lpr/lpr mice. Clues from a T cell receptor beta transgenic mouse.MRL-lpr/lpr小鼠中CD4-CD8-B220+ T细胞的起源。来自T细胞受体β转基因小鼠的线索。
J Immunol. 1993 Apr 15;150(8 Pt 1):3651-67.
9
The role of the interleukin-2 (IL-2)/IL-2 receptor pathway in MRL/lpr lymphadenopathy: the expanded CD4-8- T cell subset completely lacks functional IL-2 receptors.白细胞介素-2（IL-2）/IL-2受体通路在MRL/lpr淋巴结病中的作用：扩增的CD4 - 8 - T细胞亚群完全缺乏功能性IL-2受体。
Eur J Immunol. 1993 Jun;23(6):1378-80. doi: 10.1002/eji.1830230629.
10
Constitutive turnover of inositol-containing phospholipids in B220+ T cells from autoimmune-prone MRL-lpr/lpr mice.
J Immunol. 1990 May 15;144(10):3946-52.

引用本文的文献

1
Single-cell RNA-seq reveals disease-specific CD8+ T cell clonal expansion and a high frequency of transcriptionally distinct double-negative T cells in diabetic NOD mice.单细胞RNA测序揭示了糖尿病NOD小鼠中疾病特异性的CD8 + T细胞克隆扩增以及转录上不同的双阴性T细胞的高频率。
PLoS One. 2025 Mar 19;20(3):e0317987. doi: 10.1371/journal.pone.0317987. eCollection 2025.
2
HTLV-1 bZIP factor induces T-cell lymphoma and systemic inflammation in vivo.HTLV-1 bZIP 因子在体内诱导 T 细胞淋巴瘤和全身炎症。
PLoS Pathog. 2011 Feb 10;7(2):e1001274. doi: 10.1371/journal.ppat.1001274.
3
Autoantibody production in lpr/lpr gld/gld mice reflects accumulation of CD4+ effector cells that are resistant to regulatory T cell activity.lpr/lpr gld/gld小鼠中自身抗体的产生反映了对调节性T细胞活性具有抗性的CD4+效应细胞的积累。
J Autoimmun. 2008 Sep;31(2):98-109. doi: 10.1016/j.jaut.2008.04.022. Epub 2008 Jun 9.
4
Greatly reduced lymphoproliferation in lpr mice lacking major histocompatibility complex class I.缺乏主要组织相容性复合体I类的lpr小鼠的淋巴细胞增殖显著减少。
J Exp Med. 1995 Feb 1;181(2):641-8. doi: 10.1084/jem.181.2.641.
5
Treatment of autoimmune MRL/lpr mice with anti-B220 monoclonal antibody reduces the level of anti-DNA antibodies and lymphadenopathies.用抗B220单克隆抗体治疗自身免疫性MRL/lpr小鼠可降低抗DNA抗体水平和淋巴结病。
Immunology. 1989 Oct;68(2):204-8.
6
Subpopulations of CD4+ cells in lpr/lpr mice: differences in expression of T cell receptor/CD3 complex and proliferative responses.lpr/lpr小鼠中CD4+细胞亚群：T细胞受体/CD3复合物表达及增殖反应的差异
Clin Exp Immunol. 1990 Jul;81(1):90-6. doi: 10.1111/j.1365-2249.1990.tb05296.x.
7
Defect in negative selection in lpr donor-derived T cells differentiating in non-lpr host thymus.在非lpr宿主胸腺中分化的lpr供体来源的T细胞中，阴性选择存在缺陷。
J Exp Med. 1991 Jan 1;173(1):127-36. doi: 10.1084/jem.173.1.127.

本文引用的文献

1
Preparative nonlytic separation of Lyt2+ and Lyt2- T lymphocytes, functional analyses of the separated cells and demonstration of synergy in graft-vs.-host reaction of Lyt2+ and Lyt2- cells.Lyt2+和Lyt2- T淋巴细胞的制备性非溶细胞分离、分离细胞的功能分析以及Lyt2+和Lyt2-细胞移植物抗宿主反应中协同作用的证明。
Eur J Immunol. 1981 Mar;11(3):228-35. doi: 10.1002/eji.1830110312.
2
Flow cytometry analysis of T cells and continuous T-cell lines from autoimmune MRL/l mice.对来自自身免疫性MRL/l小鼠的T细胞和连续T细胞系进行流式细胞术分析。
Nature. 1981 Jan 22;289(5795):298-300. doi: 10.1038/289298a0.
3
Abnormalities induced by the mutant gene Ipr: expansion of a unique lymphocyte subset.由突变基因Ipr诱导的异常：一种独特淋巴细胞亚群的扩增。
J Immunol. 1982 Dec;129(6):2612-5.
4
A monoclonal antibody that recognizes B cells and B cell precursors in mice.一种识别小鼠B细胞和B细胞前体的单克隆抗体。
J Exp Med. 1981 Feb 1;153(2):269-79. doi: 10.1084/jem.153.2.269.
5
Induction of various autoantibodies by mutant gene lpr in several strains of mice.突变基因lpr在多个小鼠品系中诱导产生多种自身抗体。
J Immunol. 1984 Jul;133(1):227-33.
6
Limiting dilution analysis of interleukin 2 and colony-stimulating factor producer cells in normal and autoimmune mice.正常及自身免疫小鼠中白细胞介素2和集落刺激因子产生细胞的有限稀释分析
J Immunol. 1984 Apr;132(4):1863-8.
7
In vitro correction of the interleukin 2 defect of autoimmune mice.自身免疫小鼠白细胞介素2缺陷的体外纠正。
Eur J Immunol. 1983 Jul;13(7):601-4. doi: 10.1002/eji.1830130717.
8
Defective T cell response to presented antigen in autoimmune mice.自身免疫小鼠中T细胞对呈递抗原的反应缺陷。
J Immunol. 1984 Nov;133(5):2365-8.
9
The proliferating cells in autoimmune MRL/lpr mice lack L3T4, an antigen on "helper" T cells that is involved in the response to class II major histocompatibility antigens.自身免疫性MRL/lpr小鼠中的增殖细胞缺乏L3T4，L3T4是“辅助性”T细胞上的一种抗原，参与对II类主要组织相容性抗原的应答。
J Immunol. 1984 Jun;132(6):2686-9.
10
A rapid method for the isolation of functional thymus-derived murine lymphocytes.一种分离功能性胸腺来源的小鼠淋巴细胞的快速方法。
Eur J Immunol. 1973 Oct;3(10):645-9. doi: 10.1002/eji.1830031011.

lpr小鼠中表达B220和CD4的新型T细胞亚群：对丝裂原反应及白细胞介素-2产生存在缺陷

A new T cell subset expressing B220 and CD4 in lpr mice: defects in the response to mitogens and in the production of IL-2.

作者信息

Asano T, Tomooka S, Serushago B A, Himeno K, Nomoto K

机构信息

Department of Immunology, Kyushu University, Japan.

出版信息

Clin Exp Immunol. 1988 Oct;74(1):36-40.

PMID:2464448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1541691/
Abstract

Autoimmune-prone mice homozygous for the lpr gene develop prominent lymphadenopathy composed mainly of Thy-1+ CD8- CD4- B220+ cells. Expression patterns of B220 vs CD4 on lymph node cells from lpr mice were analysed using two-colour flow microfluorometry. B220+CD4+ cells, which were hardly seen in lymph nodes of B6-+/+ mice, increased significantly in B6-lpr mice with ageing. Functional analysis of purified B220+ CD4+ cells from lpr mice revealed that these cells scarcely responded to T cell mitogens with or without rIL-2. Furthermore, B220+ CD4+ cells were defective in IL-2 production when cultured with Con A. On the other hand, B220-CD4+ cells from B6-lpr mice showed an ability to respond to T cell mitogens similar to that of B220- CD4+ cells from B6-+/+ mice. These results indicate that an unusual T cell subset expressing both B220 and CD4 in lpr mice is functionally defective, but the intrinsic ability of B220-CD4+ cells is almost intact as compared with the counterpart in normal mice.

摘要

纯合 lpr 基因的自身免疫易感小鼠会出现明显的淋巴结病，主要由 Thy-1+ CD8- CD4- B220+ 细胞组成。使用双色流式微量荧光测定法分析了 lpr 小鼠淋巴结细胞上 B220 与 CD4 的表达模式。在 B6-+/+ 小鼠淋巴结中几乎看不到的 B220+CD4+ 细胞，在 B6-lpr 小鼠中随着年龄增长而显著增加。对来自 lpr 小鼠的纯化 B220+ CD4+ 细胞进行功能分析发现，这些细胞无论有无 rIL-2 都几乎不响应 T 细胞有丝分裂原。此外，用 Con A 培养时，B220+ CD4+ 细胞在产生 IL-2 方面存在缺陷。另一方面，B6-lpr 小鼠的 B220-CD4+ 细胞对 T 细胞有丝分裂原的反应能力与 B6-+/+ 小鼠的 B220- CD4+ 细胞相似。这些结果表明，lpr 小鼠中同时表达 B220 和 CD4 的异常 T 细胞亚群功能存在缺陷，但与正常小鼠中的对应细胞相比，B220-CD4+ 细胞的内在能力几乎完好无损。