グルココルチコイド誘導性TNFR関連タンパク質
WordNet
- reason or establish by induction
- cause to arise; "induce a crisis" (同)bring_on
- produce electric current by electrostatic or magnetic processes (同)induct
- cause to do; cause to act in a specified manner; "The ads induced me to buy a VCR"; "My children finally got me to buy a computer"; "My wife made me buy a new sofa" (同)stimulate, cause, have, get, make
- cause to occur rapidly; "the infection precipitated a high fever and allergic reactions" (同)stimulate, rush, hasten
- have or establish a relationship to; "She relates well to her peers"
- be in a relationship with; "How are these two observations related?" (同)interrelate
- give an account of; "The witness related the events"
- connected by kinship, common origin, or marriage
- being connected either logically or causally or by shared characteristics ; "painting and the related arts"; "school-related activities"; "related to micelle formation is the...ability of detergent actives to congregate at oil-water interfaces" (同)related to
- any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
- brought about or caused; not spontaneous; "a case of steroid-induced weakness"
PrepTutorEJDIC
- 〈人〉‘に'『勧めて』(…)『させる』 / …‘を'『引き起こす』,もたらす(cause) / 〈電気〉‘を'誘導する / …‘を'帰納する
- (…に)〈事件・事情など〉‘を'『物語る』《+『名』+『to』+『名』》 / (…と)…‘を'『関係させる』,結びつける《+『名』+『to(with)』+『名』》 / 〈物・事が〉(…に)関係がある,かかわる《+『to(with)』+『名(wh・節・句)』》 / (…に)〈人が〉なじむ,順応する《+『to』+『名』》
- 関係のある
- 蛋白(たんばく)質
UpToDate Contents
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English Journal
- Combined PD-1 blockade and GITR triggering induce a potent antitumor immunity in murine cancer models and synergizes with chemotherapeutic drugs.
- Lu L, Xu X, Zhang B, Zhang R, Ji H, Wang X.Author information Department of Surgical Oncology, Jindu Hospital, Nanjing 210002, China. jihongzan@126.com.AbstractBACKGROUND: The coinhibitory receptor Programmed Death-1 (PD-1) inhibits effector functions of activated T cells and prevents autoimmunity, however, cancer hijack this pathway to escape from immune attack. The costimulatory receptor glucocorticoid-induced TNFR related protein (GITR) is up-regulated on activated T cells and increases their proliferation, activation and cytokine production. We hypothesize that concomitant PD-1 blockade and GITR triggering would synergistically improve the effector functions of tumor-infiltrating T cells and increase the antitumor immunity. In present study, we evaluated the antitumor effects and mechanisms of combined PD-1 blockade and GITR triggering in a clinically highly relevant murine ID8 ovarian cancer model.
- Journal of translational medicine.J Transl Med.2014 Feb 7;12(1):36. doi: 10.1186/1479-5876-12-36.
- BACKGROUND: The coinhibitory receptor Programmed Death-1 (PD-1) inhibits effector functions of activated T cells and prevents autoimmunity, however, cancer hijack this pathway to escape from immune attack. The costimulatory receptor glucocorticoid-induced TNFR related protein (GITR) is up-regulated
- PMID 24502656
- Use of gene-modified regulatory T-cells to control autoimmune and alloimmune pathology: Is now the right time?
- Jethwa H1, Adami AA2, Maher J3.Author information 1Department of Medicine, Barnet and Chase Farm NHS Trust, Barnet, Hertfordshire EN5 3DJ, UK.2King's College London, King's Health Partners Integrated Cancer Centre, Department of Research Oncology, Guy's Hospital Campus, Great Maze Pond, London SE1 9RT, UK.3King's College London, King's Health Partners Integrated Cancer Centre, Department of Research Oncology, Guy's Hospital Campus, Great Maze Pond, London SE1 9RT, UK; Department of Immunology, Barnet and Chase Farm NHS Trust, Barnet, Hertfordshire EN5 3DJ, UK; Department of Clinical Immunology and Allergy, King's College Hospital NHS Foundation Trust, Denmark Hill, London SE5 9RS, UK. Electronic address: John.maher@kcl.ac.uk.AbstractAdoptive immunotherapy using genetically targeted T-cells has recently begun to achieve impressive clinical impact in selected tumor types. Furthermore, long-term follow-up studies indicate thus far that integrating viral vectors do not elicit clinically evident genotoxicity in T-cells, unlike hematopoietic stem cells. The optimism engendered by this clinical experience provides a platform for consideration of the extended use of this technology in other disease types. One area of particular interest entails the harnessing of regulatory T-cells (Tregs) in order to down-regulate unwanted immune responses. Increasing evidence supports the efficacy of this approach in pre-clinical models of autoimmune disease and allograft rejection. Nonetheless, questions remain about optimal host cell, transgene cargo, phenotypic stability of engineered cells in vivo and potential for toxicity. Here, we review the evidence that genetically engineered Tregs can effectively dampen pathogenic immune responses and critically evaluate the prospects for clinical development of this approach.
- Clinical immunology (Orlando, Fla.).Clin Immunol.2014 Jan;150(1):51-63. doi: 10.1016/j.clim.2013.11.004. Epub 2013 Nov 16.
- Adoptive immunotherapy using genetically targeted T-cells has recently begun to achieve impressive clinical impact in selected tumor types. Furthermore, long-term follow-up studies indicate thus far that integrating viral vectors do not elicit clinically evident genotoxicity in T-cells, unlike hemat
- PMID 24333533
- Reduced effectiveness of CD4+Foxp3+ regulatory T cells in CD28-deficient NOD.H-2h4 mice leads to increased severity of spontaneous autoimmune thyroiditis.
- Ellis JS, Hong SH, Zaghouani H, Braley-Mullen H.Author information Department of Internal Medicine, University of Missouri School of Medicine, Columbia, MO 65212;AbstractNOD.H-2h4 mice given NaI in their drinking water develop iodine-accelerated spontaneous autoimmune thyroiditis (ISAT) with chronic inflammation of the thyroid by T and B cells and production of anti-mouse thyroglobulin (MTg) autoantibody. CD28(-/-) NOD.H-2h4 mice, which have reduced numbers of CD4(+)Foxp3(+) regulatory T cells (Tregs), were developed to examine the role of Tregs in ISAT development. CD28(-/-) NOD.H2-h4 mice develop more severe ISAT than do wild-type (WT) mice, with collagen deposition (fibrosis) and low serum T4. CD28(-/-) mice have increased expression of proinflammatory cytokines IFN-γ and IL-6, consistent with increased mononuclear cell infiltration and tissue destruction in thyroids. Importantly, transferring purified CD4(+)Foxp3(+) Tregs from WT mice reduces ISAT severity in CD28(-/-) mice without increasing the total number of Tregs, suggesting that endogenous Tregs in CD28(-/-) mice are functionally ineffective. Endogenous CD28(-/-) Tregs have reduced surface expression of CD27, TNFR2 p75, and glucocorticoid-induced TNFR-related protein compared with transferred CD28(+/+) Tregs. Although anti-MTg autoantibody levels generally correlate with ISAT severity scores in WT mice, CD28(-/-) mice have lower anti-MTg autoantibody responses than do WT mice. The percentages of follicular B cells are decreased and those of marginal zone B cells are increased in spleens of CD28(-/-) mice, and they have fewer thyroid-infiltrating B cells than do WT mice. This suggests that CD28 deficiency has direct and indirect effects on the B cell compartment. B cell-deficient (B(-/-)) NOD.H-2h4 mice are resistant to ISAT, but CD28(-/-)B(-/-) mice develop ISAT comparable to WT mice and have reduced numbers of Tregs compared with WT B(-/-) mice.
- Journal of immunology (Baltimore, Md. : 1950).J Immunol.2013 Nov 15;191(10):4940-9. doi: 10.4049/jimmunol.1301253. Epub 2013 Oct 4.
- NOD.H-2h4 mice given NaI in their drinking water develop iodine-accelerated spontaneous autoimmune thyroiditis (ISAT) with chronic inflammation of the thyroid by T and B cells and production of anti-mouse thyroglobulin (MTg) autoantibody. CD28(-/-) NOD.H-2h4 mice, which have reduced numbers of CD4(+
- PMID 24098053
Related Links
- "Glucocorticoid-Induced TNFR-Related Protein" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject ... A member of the TNF receptor family that was initially identified as a ...
- Glucocorticoid-Induced TNFR-Related Protein information including symptoms, causes, diseases, symptoms, treatments, and other medical and health issues. ... Introduction: Glucocorticoid-Induced TNFR-Related Protein
★リンクテーブル★
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- 英
- glucocorticoid-induced TNFR-related protein
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- 関
- associate、association、attach、bearing、concern、connect、connection、correlate、correlation、germane、implicate、implication、interplay、link、pertain、pertinent、referable、reference、relation、relationship、relative、relevance、relevant、respect
[★]
- 誘発する、誘導する、誘起する、導入する、引き起こす
- 関
- cause、challenge、derivation、elicit、elicitation、evocation、evoke、guidance、induction、inductive、introduce、introduction、precipitate、provocation、provoke、spark
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- hypercalcaemia induced pancreatitis 高カルシウム血症による膵炎
[★]
- 関
- associated protein
[★]
腫瘍壊死因子 tumor necrosis factor