WordNet

complicated in structure; consisting of interconnected parts; "a complex set of variations based on a simple folk melody"; "a complex mass of diverse laws and customs"
a compound described in terms of the central atom to which other atoms are bound or coordinated (同)coordination_compound
a conceptual whole made up of complicated and related parts; "the complex of shopping malls, houses, and roads created a new town" (同)composite
(psychoanalysis) a combination of emotions and impulses that have been rejected from awareness but still influence a persons behavior
small room in which a monk or nun lives (同)cubicle
a device that delivers an electric current as the result of a chemical reaction (同)electric cell
a room where a prisoner is kept (同)jail cell, prison cell
(biology) the basic structural and functional unit of all organisms; they may exist as independent units of life (as in monads) or may form colonies or tissues as in higher plants and animals
any small compartment; "the cells of a honeycomb"
a small unit serving as part of or as the nucleus of a larger political movement (同)cadre
the 3rd letter of the Roman alphabet (同)c
(music) the keynote of the scale of C major
a general-purpose programing language closely associated with the UNIX operating system
any substance (as a toxin or enzyme) that stimulates an immune response in the body (especially the production of antibodies)
the 20th letter of the Roman alphabet (同)t

PrepTutorEJDIC

『いくつかの部分から成る』,複合の,合成の / 『複雑な』,入りくんだ,こみいった(complicated) / 複合体,合成物 / コンプレックス,複合(抑圧されて心に残った複雑なしこり)
(刑務所の)『独房』;(修道院の)小さい独居室 / (ミツバチの)みつ房,巣穴 / 小さい部屋 / 『細胞』 / 電池 / 花粉室 / (共産党などの)細胞
carbonの化学記号
抗原(生物の体内にはいって免疫体を作る物質)
tritiumの化学記号

UpToDate Contents

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1. 免疫不全症を引き起こすCD3／T細胞受容体複合体疾患 cd3 t cell receptor complex disorders causing immunodeficiency
2. T細胞受容体シグナル伝達 t cell receptor signaling
3. 適応細胞性免疫応答 the adaptive cellular immune response
4. T細胞受容体の遺伝学 t cell receptor genetics
5. 重度複合型免疫不全（SCID）：特定の欠損 severe combined immunodeficiency scid specific defects

English Journal

Activation of the TCR complex by small chemical compounds.

Louis-Dit-Sully C, Schamel WW.Author information Faculty of Biology, Department of Molecular Immunology, Institute of Biology III, University of Freiburg, Freiburg, Germany.AbstractSmall chemical compounds and certain metal ions can activate T cells, resulting in drug hypersensitivity reactions that are a main problem in pharmacology. Mostly, the drugs generate new antigenic epitopes on peptide-major histocompatibility complex (MHC) molecules that are recognized by the T-cell antigen receptor (TCR). In this review we discuss the molecular mechanisms of how the drugs alter self-peptide-MHC, so that neo-antigens are produced. This includes (1) haptens covalently bound to peptides presented by MHC, (2) metal ions and drugs that non-covalently bridge self-pMHC to the TCR, and (3) drugs that allow self-peptides to be presented by MHCs that otherwise are not presented. We also briefly discuss how a second signal-next to the TCR-that naïve T cells require to become activated is generated in the drug hypersensitivity reactions.
EXS.EXS.2014;104:25-39. doi: 10.1007/978-3-0348-0726-5_3.
Small chemical compounds and certain metal ions can activate T cells, resulting in drug hypersensitivity reactions that are a main problem in pharmacology. Mostly, the drugs generate new antigenic epitopes on peptide-major histocompatibility complex (MHC) molecules that are recognized by the T-cell
PMID 24214616

Activation of the TCR complex by peptide-MHC and superantigens.

Louis-Dit-Sully C, Blumenthal B, Duchniewicz M, Beck-Garcia K, Fiala GJ, Beck-García E, Mukenhirn M, Minguet S, Schamel WW.Author information Department of Molecular Immunology, Institute for Biology III, Faculty of Biology, BIOSS Center for Biological Signalling Studies, Centre for Chronic Immunodeficiency CCI, University of Freiburg and Max Planck-Institute of Immunobiology and Epigenetics, Freiburg, Germany.AbstractDrug hypersensitivity reactions are immune mediated, with T lymphocytes being stimulated by the drugs via their T-cell antigen receptor (TCR). In the nonpathogenic state, the TCR is activated by foreign peptides presented by major histocompatibility complex molecules (pMHC). Foreign pMHC binds with sufficient affinity to TCRαβ and thereby elicits phosphorylation of the cytoplasmic tails of the TCRαβ-associated CD3 subunits. The process is called TCR triggering. In this review, we discuss the current models of TCR triggering and which drug properties are crucial for TCR stimulation. The underlying molecular mechanisms mostly include pMHC-induced exposure of the CD3 cytoplasmic tails or alterations of the kinase-phosphatase equilibrium in the vicinity of CD3. In this review, we also discuss triggering of the TCR by small chemical compounds in context of these general mechanisms.
EXS.EXS.2014;104:9-23. doi: 10.1007/978-3-0348-0726-5_2.
Drug hypersensitivity reactions are immune mediated, with T lymphocytes being stimulated by the drugs via their T-cell antigen receptor (TCR). In the nonpathogenic state, the TCR is activated by foreign peptides presented by major histocompatibility complex molecules (pMHC). Foreign pMHC binds with
PMID 24214615

Selective activation of antigen-experienced T cells by anti-CD3 constrained on nanoparticles.

Lo YC, Edidin MA, Powell JD.Author information Department of Pharmacology and Molecular Sciences, School of Medicine, Johns Hopkins University, Baltimore, MD 21231;AbstractActivation of T cells through the TCR is mediated by the TCR-CD3 signaling complex. Cross linking of this complex with Abs directed against CD3 leads to potent activation of T cells. However, such activation is not Ag-specific. We exploited the observation that the TCR-CD3 complex is clustered on T cells that have been activated by Ag by using anti-CD3 nanoparticles to selectively activate Ag-experienced mouse T cells. We find that constraining anti-CD3 on the surface of a nanoparticle markedly and selectively enhances proliferation and cytokine production of Ag-experienced T cells but does not activate naive T cells. This effect was recapitulated in heterogeneous cultures containing mixtures of Ag-specific CD4(+) or CD8(+) T cells and bystander T cells. Furthermore, in vivo anti-CD3-coated nanoparticles increased the expansion of Ag-specific T cells following vaccination. Overall, these findings indicate that anti-CD3-coated nanoparticles could be use to enhance the efficacy of vaccines and immunotherapy. The results also suggest constraining a ligand on the surface of a nanoparticle might as general strategy for selectively targeting clustered receptors.
Journal of immunology (Baltimore, Md. : 1950).J Immunol.2013 Nov 15;191(10):5107-14. doi: 10.4049/jimmunol.1301433. Epub 2013 Oct 4.
Activation of T cells through the TCR is mediated by the TCR-CD3 signaling complex. Cross linking of this complex with Abs directed against CD3 leads to potent activation of T cells. However, such activation is not Ag-specific. We exploited the observation that the TCR-CD3 complex is clustered on T
PMID 24098054

Japanese Journal

リンパ球における非神経性コリン作動系の発見とその生理的役割の解析

藤井健志
日本薬理学雑誌 : FOLIA PHARMACOLOGICA JAPONICA 123(3), 179-188, 2004-03-01
… いる．T細胞受容体/CD3複合体を介するT細胞の活性化，T細胞と抗原提示細胞との接触，あるいはT細胞におけるアデニル酸シクラーゼ経路の活性化は，ChATおよびM5 mAChR遺伝子発現の増強をもたらし，T細胞のコリン作動系を活性化させる．ACh作用薬によるmAChR刺激は，主にM3およびM5 mAChRを介して，Tおよ …
NAID 10017019185