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1
Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.抗原呈递细胞在接触性超敏反应的发生和持续中的作用。
J Exp Med. 1980 Feb 1;151(2):362-75. doi: 10.1084/jem.151.2.362.
2
Specialized antigen-presenting cells. Splenic dendritic cells and peritoneal-exudate cells induced by mycobacteria activate effector T cells that are resistant to suppression.特异性抗原呈递细胞。由分枝杆菌诱导产生的脾脏树突状细胞和腹腔渗出细胞可激活对抑制具有抗性的效应T细胞。
J Exp Med. 1982 May 1;155(5):1344-56. doi: 10.1084/jem.155.5.1344.
3
Intracameral injection of antigen potentiates the production of antigen-specific T cell proteins in serum after the induction of delayed-type hypersensitivity.在前房内注射抗原可增强迟发型超敏反应诱导后血清中抗原特异性T细胞蛋白的产生。
Invest Ophthalmol Vis Sci. 1995 Jun;36(7):1470-6.
4
Macrophages play an essential role in antigen-specific immune suppression mediated by T CD8⁺ cell-derived exosomes.巨噬细胞在由T CD8⁺细胞衍生的外泌体介导的抗原特异性免疫抑制中发挥着重要作用。
Immunology. 2015 Sep;146(1):23-32. doi: 10.1111/imm.12466. Epub 2015 Apr 27.
5
Induced suppression of the efferent phase of contact sensitivity in rats.诱导大鼠接触敏感性传出相的抑制。
Cell Immunol. 1990 Oct 15;130(2):378-88. doi: 10.1016/0008-8749(90)90280-5.
6
Cell surface expression of I-A products is required for contact sensitivity induction by trinitrophenyl-coupled epidermal cells.三硝基苯基偶联的表皮细胞诱导接触敏感性需要I-A产物的细胞表面表达。
Microbiol Immunol. 1981;25(12):1335-44. doi: 10.1111/j.1348-0421.1981.tb00142.x.
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Heme oxygenase (HO-1) is involved in the negative regulation of contact sensitivity reaction.血红素加氧酶(HO-1)参与接触性敏感反应的负调控。
Pharmacol Rep. 2008 Nov-Dec;60(6):933-40.
8
Distinct populations of antigen-presenting macrophages are required for induction of effector and regulatory cells in contact sensitivity response in mice.在小鼠接触性超敏反应中,诱导效应细胞和调节性细胞需要不同群体的抗原呈递巨噬细胞。
J Leukoc Biol. 1993 Mar;53(3):320-6. doi: 10.1002/jlb.53.3.320.
9
Distinctive immunological properties of cultured murine thymic epithelial cells.培养的小鼠胸腺上皮细胞的独特免疫学特性。
Clin Immunol Immunopathol. 1984 Feb;30(2):227-32. doi: 10.1016/0090-1229(84)90057-6.
10
Mechanism of action of a T suppressor factor (TsF) in contact sensitivity: the T cell target for TsF activity in adoptive transfer of immunity is not effector cell.T抑制因子(TsF)在接触敏感性中的作用机制:在免疫的过继转移中,TsF活性的T细胞靶标不是效应细胞。
J Immunol. 1986 Sep 15;137(6):1829-35.

引用本文的文献

1
Dendritic cells and T cells transfer sensitization for delayed-type hypersensitivity after skin painting with contact sensitizer.在用接触致敏剂进行皮肤涂抹后,树突状细胞和T细胞会传递迟发型超敏反应的致敏作用。
Immunology. 1989 Jan;66(1):96-9.
2
Human T lymphocyte priming in vitro by haptenated autologous dendritic cells.半抗原化自体树突状细胞在体外对人T淋巴细胞的致敏作用。
Clin Exp Immunol. 1999 Aug;117(2):209-16. doi: 10.1046/j.1365-2249.1999.00958.x.
3
Contact dermatitis. Clinical perspectives and basic mechanisms.接触性皮炎。临床观点与基本机制。
Clin Rev Allergy Immunol. 1996 Summer;14(2):151-84. doi: 10.1007/BF02780197.
4
The skin as an immune organ.皮肤作为一个免疫器官。
West J Med. 1994 Feb;160(2):146-52.
5
Induction of contact sensitivity and antigenic competition by the intravenous administration of contact sensitizers.通过静脉注射接触致敏剂诱导接触敏感性和抗原竞争。
Immunology. 1981 Jan;42(1):111-8.
6
Reactivity of Langerhans cells with hybridoma antibody.朗格汉斯细胞与杂交瘤抗体的反应性。
Proc Natl Acad Sci U S A. 1981 Apr;78(4):2541-4. doi: 10.1073/pnas.78.4.2541.
7
Sensitization or tolerance to Mycobacterium leprae antigen by route of injection.通过注射途径对麻风分枝杆菌抗原产生致敏或耐受。
Infect Immun. 1982 Nov;38(2):673-80. doi: 10.1128/iai.38.2.673-680.1982.
8
Specialized antigen-presenting cells. Splenic dendritic cells and peritoneal-exudate cells induced by mycobacteria activate effector T cells that are resistant to suppression.特异性抗原呈递细胞。由分枝杆菌诱导产生的脾脏树突状细胞和腹腔渗出细胞可激活对抑制具有抗性的效应T细胞。
J Exp Med. 1982 May 1;155(5):1344-56. doi: 10.1084/jem.155.5.1344.
9
Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.抗原和受体驱动的调节机制。III. 用抗交叉反应性独特型抗体诱导对偶氮苯砷酸盐的迟发型超敏反应。
J Exp Med. 1980 Apr 1;151(4):896-909. doi: 10.1084/jem.151.4.896.
10
Prolongation of skin graft survival in mice by in vitro PUVA treatment and failure of induction of specific immunological memory by PUVA-treated grafts.通过体外补骨脂素加长波紫外线(PUVA)治疗延长小鼠皮肤移植存活时间以及经PUVA处理的移植物诱导特异性免疫记忆失败
Arch Dermatol Res. 1984;276(2):82-5. doi: 10.1007/BF00511060.

本文引用的文献

1
Antitrinitrophenyl (TNP) plaque assay. Primary response of Balb/c mice to soluble and particulate immunogen.抗三硝基苯基(TNP)空斑试验。Balb/c小鼠对可溶性和颗粒性免疫原的初次反应。
Proc Soc Exp Biol Med. 1969 Nov;132(2):575-81. doi: 10.3181/00379727-132-34264.
2
The induction of delayed hypersensitivity by macrophage-associated antigen. The role of macrophage cytophilic antibody.巨噬细胞相关抗原诱导迟发型超敏反应。巨噬细胞嗜细胞抗体的作用。
Immunology. 1974 Mar;26(3):465-76.
3
The interaction of particulate horseradish peroxidase (HRP)-anti HRP immune complexes with mouse peritoneal macrophages in vitro.颗粒性辣根过氧化物酶(HRP)-抗HRP免疫复合物与小鼠腹腔巨噬细胞在体外的相互作用。
J Cell Biol. 1972 Dec;55(3):616-34. doi: 10.1083/jcb.55.3.616.
4
The modifying effect of BCG on the immunological induction of T cells.卡介苗对T细胞免疫诱导的调节作用。
J Exp Med. 1974 Jun 1;139(6):1540-52. doi: 10.1084/jem.139.6.1540.
5
Serologically demonstrable alloantigens of mouse epidermal cells.小鼠表皮细胞的血清学可证实同种抗原
J Exp Med. 1972 Apr 1;135(4):938-55. doi: 10.1084/jem.135.4.938.
6
Contact and delayed hypersensitivity in the mouse. I. Active sensitization and passive transfer.小鼠的接触性和迟发型超敏反应。I. 主动致敏和被动转移。
Immunology. 1968 Sep;15(3):405-16.
7
Immuno-regulatory role of spleen localizing thymocytes.脾脏定位胸腺细胞的免疫调节作用。
J Immunol. 1974 Feb;112(2):546-54.
8
Contact sensitivity to oxazolone in the mouse. VIII. Demonstration of several classes of antibody in the sera of contact sensitized and unimmunized mice by a simplified antiglobulin assay.小鼠对恶唑酮的接触性敏感。VIII. 通过简化抗球蛋白测定法证明接触致敏和未免疫小鼠血清中的几类抗体
Immunology. 1972 Sep;23(3):289-98.
9
Augmentation of delayed-type hypersensitivity by doses of cyclophosphamide which do not affect antibody responses.不影响抗体反应的环磷酰胺剂量增强迟发型超敏反应。
J Exp Med. 1975 Mar 1;141(3):697-702. doi: 10.1084/jem.141.3.697.
10
A stable form of delayed-type hypersensitivity.一种稳定形式的迟发型超敏反应。
J Exp Med. 1975 Jan 1;141(1):82-96. doi: 10.1084/jem.141.1.82.

抗原呈递细胞在接触性超敏反应的发生和持续中的作用。

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

作者信息

Ptak W, Rozycka D, Askenase P W, Gershon R K

出版信息

J Exp Med. 1980 Feb 1;151(2):362-75. doi: 10.1084/jem.151.2.362.

DOI:10.1084/jem.151.2.362
PMID:7356727
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2185775/
Abstract

Three outcomes pertinent to contact sensitivity (CS) follow immunization with various forms of trinitrophenylated (TNP) substrates: (a) specific immunological unresponsiveness for CS is induced when immunization favors activation of splenic suppressor cells. This state is achieved by intravenous injection of trinitrophenyl-conjugated to various types of cells, such as peritoneal exudate cells (PEC). (b) A short-lived or evanescent form of CS is induced when immunization reduces activation of the suppressor circuit. This can be achieved by subcutaneous immunization with trinitrophenyl conjugated to syngeneic PEC, by pretreatment with cyclophosphamide to diminish suppression before intravenous immunization, or by altering the mode of antigen presentation by using TNP-substrate that has undergone phagocytosis. (c) A long-lived form of CS is induced when trinitrophenyl is presented to the immune system on skin cells either by contact skin painting with reactive trinitrophenyl, or by subcutaneous, or even intravenous injection of trinitrophenyl-conjugated epidermal cells. In fact, trinitrophenyl-conjugated epidermal cells induced CS even when the suppressor circuit was activated by intravenous coadministration of TNP-PEC. This implies that antigen presentation on epidermal cells induces sensitized cells that are relatively resistant to suppression. The cell type(s) in the skin that are primarily responsible for this potent form of antigen presentation are most likely Langerhans cells, because they can be concentrated by virtue of their Fc receptors and they are Ia positive. Thus, both the anatomical site where antigen is first encountered by the immune apparatus, as well as the nature of the cells which present the antigen, determine whether a CS response will ensue, as well as whether it will be evanescent or long-lasting.

摘要

用各种形式的三硝基苯基化(TNP)底物进行免疫后,会出现与接触性敏感(CS)相关的三种结果:(a)当免疫有利于脾抑制细胞激活时,会诱导出对CS的特异性免疫无反应性。通过静脉注射与各种类型细胞(如腹膜渗出细胞[PEC])结合的三硝基苯基可达到这种状态。(b)当免疫降低抑制回路的激活时,会诱导出一种短暂或易消逝形式的CS。这可通过皮下注射与同基因PEC结合的三硝基苯基、在静脉免疫前用环磷酰胺预处理以减少抑制作用,或通过使用已被吞噬的TNP底物改变抗原呈递方式来实现。(c)当通过用反应性三硝基苯基接触皮肤涂漆,或通过皮下甚至静脉注射三硝基苯基化的表皮细胞,将三硝基苯基呈递给免疫系统时,会诱导出一种持久形式的CS。事实上,即使通过静脉共同给予TNP - PEC激活了抑制回路,三硝基苯基化的表皮细胞仍能诱导CS。这意味着表皮细胞上的抗原呈递会诱导出相对抗抑制的致敏细胞。皮肤中主要负责这种强效抗原呈递形式的细胞类型很可能是朗格汉斯细胞,因为它们可凭借其Fc受体进行富集且Ia呈阳性。因此,免疫装置首次遇到抗原的解剖部位以及呈递抗原的细胞性质,决定了是否会引发CS反应,以及该反应是短暂的还是持久的。