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Experimental cutaneous leishmaniasis: induction and regulation of T cells following infection of mice with Leishmania major.

作者信息

Scott P, Farrell J P

机构信息

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA.

出版信息

Chem Immunol. 1998;70:60-80. doi: 10.1159/000058698.

DOI:10.1159/000058698
PMID:9509670
Abstract
摘要

相似文献

1
Experimental cutaneous leishmaniasis: induction and regulation of T cells following infection of mice with Leishmania major.
Chem Immunol. 1998;70:60-80. doi: 10.1159/000058698.
2
Resistance to Leishmania major in mice.小鼠对硕大利什曼原虫的抗性。
Science. 1996 Nov 22;274(5291):1392-3.
3
Genetic control of the T cell response to Leishmania major infection.T细胞对利什曼原虫主要感染反应的遗传控制。
Adv Exp Med Biol. 1998;452:61-6. doi: 10.1007/978-1-4615-5355-7_8.
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The role of IL-12 in regulation of T helper cell subsets in vivo. Lessons from experimental cutaneous leishmaniasis.白细胞介素-12在体内调节辅助性T细胞亚群中的作用。来自实验性皮肤利什曼病的经验教训。
Ann N Y Acad Sci. 1996 Oct 31;795:250-6. doi: 10.1111/j.1749-6632.1996.tb52674.x.
5
JNK1 is required for T cell-mediated immunity against Leishmania major infection.JNK1是T细胞介导的针对硕大利什曼原虫感染的免疫反应所必需的。
J Immunol. 2000 Sep 1;165(5):2671-6. doi: 10.4049/jimmunol.165.5.2671.
6
Leishmania major: effect of infectious dose on T cell subset development in BALB/c mice.硕大利什曼原虫:感染剂量对BALB/c小鼠T细胞亚群发育的影响
Exp Parasitol. 1996 Nov;84(2):124-35. doi: 10.1006/expr.1996.0098.
7
Interaction between the innate and the acquired immune system following infection of different mouse strains with Leishmania major.用硕大利什曼原虫感染不同小鼠品系后,先天免疫系统与获得性免疫系统之间的相互作用。
Ann N Y Acad Sci. 1994 Aug 15;730:84-92. doi: 10.1111/j.1749-6632.1994.tb44241.x.
8
T cells from Leishmania major-susceptible BALB/c mice have a defect in efficiently up-regulating CXCR3 upon activation.来自对硕大利什曼原虫易感的BALB/c小鼠的T细胞在激活后有效上调CXCR3方面存在缺陷。
J Immunol. 2008 Oct 1;181(7):4613-20. doi: 10.4049/jimmunol.181.7.4613.
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Immunology of murine leishmaniasis.小鼠利什曼病的免疫学
Clin Dermatol. 1996 Sep-Oct;14(5):451-64. doi: 10.1016/0738-081x(96)00037-5.
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An immunomodulatory function for neutrophils during the induction of a CD4+ Th2 response in BALB/c mice infected with Leishmania major.在感染硕大利什曼原虫的BALB/c小鼠中,中性粒细胞在诱导CD4+ Th2反应过程中的免疫调节功能。
J Immunol. 2000 Sep 1;165(5):2628-36. doi: 10.4049/jimmunol.165.5.2628.

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Comparative analysis of the tissue inflammatory response in human cutaneous and disseminated leishmaniasis.
人类皮肤利什曼病和播散性利什曼病组织炎症反应的比较分析。
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Altered dendritic cell phenotype in response to Leishmania amazonensis amastigote infection is mediated by MAP kinase, ERK.响应亚马逊利什曼原虫无鞭毛体感染而改变的树突状细胞表型是由丝裂原活化蛋白激酶ERK介导的。
Am J Pathol. 2009 May;174(5):1818-26. doi: 10.2353/ajpath.2009.080905. Epub 2009 Apr 6.
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Functional dichotomy of dendritic cells following interaction with Leishmania braziliensis: infected cells produce high levels of TNF-alpha, whereas bystander dendritic cells are activated to promote T cell responses.与巴西利什曼原虫相互作用后树突状细胞的功能二分法:被感染的细胞产生高水平的肿瘤坏死因子-α,而旁观者树突状细胞被激活以促进T细胞反应。
J Immunol. 2008 Nov 1;181(9):6473-80. doi: 10.4049/jimmunol.181.9.6473.
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Leishmania major: common antigen responsible for induction of delayed-type hypersensitivity response in guinea pigs.
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Antigen-responsive CD4+ T cells from C3H mice chronically infected with Leishmania amazonensis are impaired in the transition to an effector phenotype.来自慢性感染亚马逊利什曼原虫的C3H小鼠的抗原反应性CD4 + T细胞向效应表型的转变受损。
Infect Immun. 2006 Mar;74(3):1547-54. doi: 10.1128/IAI.74.3.1547-1554.2006.
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Inbred strains derived from feral mice reveal new pathogenic mechanisms of experimental leishmaniasis due to Leishmania major.源自野生小鼠的近交系揭示了由硕大利什曼原虫引起的实验性利什曼病的新致病机制。
Infect Immun. 2004 Aug;72(8):4603-11. doi: 10.1128/IAI.72.8.4603-4611.2004.
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T-cell-mediated immune responses in patients with cutaneous or mucosal leishmaniasis: long-term evaluation after therapy.皮肤或黏膜利什曼病患者的T细胞介导的免疫反应:治疗后的长期评估
Clin Diagn Lab Immunol. 2002 Mar;9(2):251-6. doi: 10.1128/cdli.9.2.251-256.2002.
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Influence of parasite load on the ability of type 1 T cells to control Leishmania major infection.寄生虫负荷对1型T细胞控制硕大利什曼原虫感染能力的影响。
Infect Immun. 2002 Feb;70(2):498-503. doi: 10.1128/IAI.70.2.498-503.2002.