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1
Genetic control of immunoregulatory circuits. Genes linked to the Ig locus govern communication between regulatory T-cell sets.免疫调节回路的基因控制。与免疫球蛋白（Ig）基因座相关的基因调控调节性T细胞亚群之间的通讯。
J Exp Med. 1979 Jul 1;150(1):44-50. doi: 10.1084/jem.150.1.44.
2
H-2-linked Ir gene control of VH determinant(s)-specific helper T cells.H-2连锁Ir基因对VH决定簇特异性辅助性T细胞的控制。
J Mol Cell Immunol. 1986;2(5):255-64.
3
Influence of Igh-C- and MHC-linked genes on the activity of immunoglobulin-recognizing T cells.免疫球蛋白重链恒定区（Igh-C）基因和主要组织相容性复合体（MHC）相关基因对免疫球蛋白识别性T细胞活性的影响。
J Immunol. 1983 Jul;131(1):103-8.
4
Immunoregulatory circuits among T-cell sets. I. T-helper cells induce other T-cell sets to exert feedback inhibition.T细胞亚群间的免疫调节环路。I.辅助性T细胞诱导其他T细胞亚群发挥反馈抑制作用。
J Exp Med. 1978 Apr 1;147(4):1106-15. doi: 10.1084/jem.147.4.1106.
5
Tolerance for self IG at the level of the Ly1+ T cell.Ly1+ T细胞水平对自身免疫球蛋白的耐受性。
J Exp Med. 1983 Dec 1;158(6):1868-80. doi: 10.1084/jem.158.6.1868.
6
Idiotypes and allotypes on Ia-binding alloactivated Lyt-1+,2-,3- T cells are coded for by genes linked to the igh-1 allotype locus.与Ia结合的同种异体活化的Lyt-1⁺、2⁻、3⁻ T细胞上的独特型和同种异型由与igh-1同种异型基因座连锁的基因编码。
J Immunol. 1983 Mar;130(3):1426-31.
7
Mechanisms of Ly2 suppressor cell activity. Activation of an Ly1 I-J+ cell is required to transduce the suppressive signal.Ly2抑制性细胞活性的机制。转导抑制信号需要激活Ly1 I-J+细胞。
J Exp Med. 1984 May 1;159(5):1413-28. doi: 10.1084/jem.159.5.1413.
8
Priming of T helper cells by antigen-activated B cells. B cell-primed Lyt-1+ helper cells are restricted to cooperate with B cells expressing the IgvH phenotype of the priming B cells.抗原激活的B细胞对辅助性T细胞的致敏作用。经B细胞致敏的Lyt-1⁺辅助性细胞只能与表达致敏B细胞IgvH表型的B细胞协同作用。
J Exp Med. 1981 May 1;153(5):1236-45. doi: 10.1084/jem.153.5.1236.
9
T cell allotypic determinants encoded by genes linked to the immunoglobulin heavy chain locus. I. Establishment of monoclonal antibodies against allotypic determinants.由与免疫球蛋白重链基因座连锁的基因编码的T细胞同种异型决定簇。I. 针对同种异型决定簇的单克隆抗体的建立。
J Immunol. 1983 Jun;130(6):2920-5.
10
Influence of IgH V-region genes on the growth kinetics of a murine B cell leukemia (BCL1).免疫球蛋白重链可变区基因对小鼠B细胞白血病（BCL1）生长动力学的影响。
J Immunol. 1981 Jan;126(1):54-8.

引用本文的文献

1
Special regulatory T-cell review: A rose by any other name: from suppressor T cells to Tregs, approbation to unbridled enthusiasm.特殊调节性T细胞综述：换个名字的玫瑰：从抑制性T细胞到调节性T细胞，从认可到过度热情。
Immunology. 2008 Jan;123(1):20-7. doi: 10.1111/j.1365-2567.2007.02779.x.
2
Expression of an idiotype (Id-460) during in vivo anti-dinitrophenyl antibody responses. II. Transient idiotypic dominance.体内抗二硝基苯基抗体应答过程中独特型（Id-460）的表达。II. 短暂的独特型优势。
J Exp Med. 1981 Nov 1;154(5):1432-41. doi: 10.1084/jem.154.5.1432.
3
Two Ly-2 T helper cell subsets distinguished by Qa-1 phenotype. The priming environment determines whether one or both subsets will be generated.通过Qa-1表型区分的两个Ly-2辅助性T细胞亚群。启动环境决定是否会产生一个或两个亚群。
J Exp Med. 1982 Mar 1;155(3):831-8. doi: 10.1084/jem.155.3.831.
4
A mathematical model of B lymphocyte differentiation: control by antigen.B淋巴细胞分化的数学模型：受抗原控制。
J Math Biol. 1981;13(1):67-86. doi: 10.1007/BF00276866.
5
Selective suppression of the major idiotypic component of an antihapten response by soluble T cell-derived factors with idiotypic or anti-idiotypic receptors.利用具有独特型或抗独特型受体的可溶性T细胞衍生因子选择性抑制抗半抗原反应的主要独特型成分。
J Exp Med. 1980 May 1;151(5):1213-31. doi: 10.1084/jem.151.5.1213.
6
Non-H-2 restriction of expression of passively transferred delayed sensitivity.被动转移迟发型超敏反应表达的非H-2限制
J Exp Med. 1982 May 1;155(5):1334-43. doi: 10.1084/jem.155.5.1334.
7
Helper and suppressor T cell factors.辅助性和抑制性T细胞因子。
Springer Semin Immunopathol. 1980 May;3(1):93-127. doi: 10.1007/BF00199927.
8
IgG heavy chain allotypes (Gm) in autoimmune diseases.自身免疫性疾病中的IgG重链同种异型（Gm）
Clin Exp Immunol. 1980 Oct;42(1):20-6.
9
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. IX. Characterization of Idiotype-specific effector-phase suppressor cells on plaque-forming cell responses in vitro.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。IX. 体外针对空斑形成细胞应答的独特型特异性效应期抑制细胞的特性
J Exp Med. 1981 Jun 1;153(6):1445-56. doi: 10.1084/jem.153.6.1445.
10
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VIII. Suppressor cell pathways in cutaneous sensitivity responses.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞反应。VIII. 皮肤敏感性反应中的抑制细胞途径。
J Exp Med. 1981 Apr 1;153(4):811-22. doi: 10.1084/jem.153.4.811.

本文引用的文献

1
Immunization of dissociated spleen cell cultures from normal mice.对来自正常小鼠的脾细胞解离培养物进行免疫接种。
J Exp Med. 1967 Sep 1;126(3):423-42. doi: 10.1084/jem.126.3.423.
2
Separation of helper T cells from suppressor T cells expressing different Ly components. II. Activation by antigen: after immunization, antigen-specific suppressor and helper activities are mediated by distinct T-cell subclasses.表达不同Ly成分的辅助性T细胞与抑制性T细胞的分离。II. 抗原激活：免疫后，抗原特异性抑制和辅助活性由不同的T细胞亚类介导。
J Exp Med. 1976 Jun 1;143(6):1391-40. doi: 10.1084/jem.143.6.1391.
3
The function and interrelationships of T-cell receptors, Ir genes and other histocompatibility gene products.T细胞受体、免疫反应基因及其他组织相容性基因产物的功能与相互关系。
Transplant Rev. 1975;22:175-95. doi: 10.1111/j.1600-065x.1975.tb01559.x.
4
On the structure of the T-cell receptor for antigen.关于抗原T细胞受体的结构
Cold Spring Harb Symp Quant Biol. 1977;41 Pt 1:285-94. doi: 10.1101/sqb.1977.041.01.034.
5
Antigen-binding, idiotypic receptors from T lymphocytes: an analysis of their biochemistry, genetics, and use as immunogens to produce specific immune tolerance.T淋巴细胞的抗原结合型独特型受体：对其生物化学、遗传学及用作免疫原以产生特异性免疫耐受的分析
Cold Spring Harb Symp Quant Biol. 1977;41 Pt 1:275-84. doi: 10.1101/sqb.1977.041.01.033.
6
"Panning" for lymphocytes: a method for cell selection.“淘选”淋巴细胞：一种细胞选择方法。
Proc Natl Acad Sci U S A. 1978 Jun;75(6):2844-8. doi: 10.1073/pnas.75.6.2844.
7
Functional specificity of thymus- dependent lymphocytes.胸腺依赖性淋巴细胞的功能特异性。
Science. 1977 Mar 25;195(4284):1293-300. doi: 10.1126/science.320663.
8
Immunoregulatory circuits among T-cell sets. Identification of a subpopulation of T-helper cells that induces feedback inhibition.T细胞集之间的免疫调节回路。诱导反馈抑制的辅助性T细胞亚群的鉴定。
J Exp Med. 1978 Oct 1;148(4):871-7. doi: 10.1084/jem.148.4.871.
9
Idiotype-specific T helper cells are required to induce idiotype-positive B memory cells to secrete antibody.诱导独特型阳性B记忆细胞分泌抗体需要独特型特异性辅助性T细胞。
Eur J Immunol. 1978 Aug;8(8):600-6. doi: 10.1002/eji.1830080812.
10
Immunoregulatory circuits among T-cell sets. II. Physiologic role of feedback inhibition in vivo: absence in NZB mice.T细胞集之间的免疫调节回路。II. 体内反馈抑制的生理作用：NZB小鼠中不存在。
J Exp Med. 1978 Apr 1;147(4):1116-25. doi: 10.1084/jem.147.4.1116.

免疫调节回路的基因控制。与免疫球蛋白（Ig）基因座相关的基因调控调节性T细胞亚群之间的通讯。

Genetic control of immunoregulatory circuits. Genes linked to the Ig locus govern communication between regulatory T-cell sets.

作者信息

Eardley D D, Shen F W, Cantor H, Gershon R K

出版信息

J Exp Med. 1979 Jul 1;150(1):44-50. doi: 10.1084/jem.150.1.44.

DOI:10.1084/jem.150.1.44
PMID:109574
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2185604/
Abstract

Antigen-stimulated Ly1:Qa1+ cells induce a nonimmune set of T-acceptor cells (surface phenotype Ly123+Qa1+) to participate in the generation of specific suppressive activity. The experiments reported here were designed to test the possibility that the interaction between T-inducer and T-acceptor cells might be governed by genes linked to the Ig locus. We find that inducer:acceptor interactions occur only if the inducer and acceptor T-cell sets are obtained from donor that are identical at the Ig locus and are independent of the Ig locus expressed on the B cells used for assay of T-helper activity. In addition, experiments using inducer and acceptor T cells from the congenic recombinant BAB. 14 strain show that T-T interactions are not governed by Ig-CH genes, per se. These data indicate that T-inducer: T-acceptor interactions are governed by Ig-linked genes that may control expression of VH-like structures on T cells, or control expression of as yet unidentified cell-surface molecules.

摘要

抗原刺激的Ly1:Qa1+细胞诱导一组非免疫性的T受体细胞（表面表型为Ly123+Qa1+）参与特异性抑制活性的产生。本文报道的实验旨在测试T诱导细胞与T受体细胞之间的相互作用可能受与Ig基因座连锁的基因调控的可能性。我们发现，只有当诱导细胞和受体T细胞系来自在Ig基因座上相同的供体，并且独立于用于检测T辅助活性的B细胞上表达的Ig基因座时，诱导细胞与受体细胞之间才会发生相互作用。此外，使用来自同源重组BAB.14品系的诱导细胞和受体T细胞进行的实验表明，T-T相互作用本身不受Ig-CH基因的调控。这些数据表明，T诱导细胞与T受体细胞之间的相互作用受与Ig连锁的基因调控，这些基因可能控制T细胞上类VH结构的表达，或控制尚未鉴定的细胞表面分子的表达。