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在缺乏B细胞的情况下针对硕大利什曼原虫的极化辅助性T细胞应答

Polarized helper-T-cell responses against Leishmania major in the absence of B cells.

作者信息

Brown D R, Reiner S L

机构信息

Committee on Immunology, The University of Chicago, Illinois 60637, USA.

出版信息

Infect Immun. 1999 Jan;67(1):266-70. doi: 10.1128/IAI.67.1.266-270.1999.

DOI:10.1128/IAI.67.1.266-270.1999
PMID:9864225
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC96306/
Abstract

B-cell-to-T-cell signaling can shape helper T (Th) cell responses. During infection with Leishmania major, Th response is critical in determining the outcome of disease. Resistance depends on the generation of a protective Th1 response, while susceptibility is mediated by the generation of a Th2 response. In this study, we determined whether B cells are required for the development of polarized Th1 and Th2 responses during infection with L. major. Mice lacking B cells due to disruption of the immunoglobulin M locus (microMT) were infected with L. major, and disease progression and Th cell development were assessed. On the genetically resistant C57BL background, both wild-type and microMT mice controlled the infection and mounted a Th1 response. On the genetically susceptible BALB/c background, both wild-type and microMT mice were susceptible to infection and generated Th2 responses. Thus, during L. major infection, neither direct antigen presentation or costimulation by B cells nor antibody-mediated effector functions are essential for the development of polarized Th responses.

摘要

B细胞向T细胞的信号传导可塑造辅助性T(Th)细胞反应。在感染硕大利什曼原虫期间,Th反应对于决定疾病的转归至关重要。抵抗力取决于保护性Th1反应的产生,而易感性则由Th2反应的产生介导。在本研究中,我们确定了在感染硕大利什曼原虫期间,极化的Th1和Th2反应的发展是否需要B细胞。因免疫球蛋白M基因座(microMT)破坏而缺乏B细胞的小鼠感染了硕大利什曼原虫,并评估了疾病进展和Th细胞发育。在遗传抗性C57BL背景下,野生型和microMT小鼠均控制了感染并产生了Th1反应。在遗传易感的BALB/c背景下,野生型和microMT小鼠均易受感染并产生Th2反应。因此,在感染硕大利什曼原虫期间,B细胞的直接抗原呈递或共刺激以及抗体介导的效应功能对于极化Th反应的发展均不是必需的。

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本文引用的文献

1
Cytokines induce the development of functionally heterogeneous T helper cell subsets.细胞因子诱导功能异质性T辅助细胞亚群的发育。
Immunity. 1998 Mar;8(3):275-83. doi: 10.1016/s1074-7613(00)80533-6.
2
Role of B-cell and Fc receptors in the selection of T-cell epitopes.B细胞和Fc受体在T细胞表位选择中的作用。
Curr Opin Immunol. 1998 Feb;10(1):88-92. doi: 10.1016/s0952-7915(98)80037-x.
3
Antigen-primed T cells from B cell-deficient JHD mice fail to provide B cell help.来自B细胞缺陷型JHD小鼠的抗原致敏T细胞无法提供B细胞辅助。
J Immunol. 1998 Feb 15;160(4):1694-700.
4
A role for B cells in the development of T cell helper function in a malaria infection in mice.B细胞在小鼠疟疾感染中T细胞辅助功能发育中的作用。
Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1730-4. doi: 10.1073/pnas.95.4.1730.
5
CD4+ T cell-mediated granulomatous pathology in schistosomiasis is downregulated by a B cell-dependent mechanism requiring Fc receptor signaling.血吸虫病中CD4 + T细胞介导的肉芽肿病理通过一种依赖B细胞的机制被下调,该机制需要Fc受体信号传导。
J Exp Med. 1998 Feb 16;187(4):619-29. doi: 10.1084/jem.187.4.619.
6
In infection with Schistosoma mansoni, B cells are required for T helper type 2 cell responses but not for granuloma formation.在曼氏血吸虫感染中,2型辅助性T细胞反应需要B细胞参与,但肉芽肿形成则不需要。
J Immunol. 1997 May 15;158(10):4832-7.
7
Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.在B细胞缺陷小鼠的肺部和气道中会发生富含嗜酸性粒细胞的过敏性炎症。
J Exp Med. 1997 Mar 3;185(5):885-92. doi: 10.1084/jem.185.5.885.
8
Evidence for B cell participation in the in vitro and in vivo maintenance of in vivo staphylococcal enterotoxin B-induced T cell anergy.B细胞参与体内葡萄球菌肠毒素B诱导的T细胞无反应性的体外和体内维持的证据。
Int Immunol. 1997 Jan;9(1):65-72. doi: 10.1093/intimm/9.1.65.
9
Allergic airway sensitization induces T cell activation but not airway hyperresponsiveness in B cell-deficient mice.变应性气道致敏可诱导B细胞缺陷小鼠的T细胞活化,但不会导致气道高反应性。
Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1350-5. doi: 10.1073/pnas.94.4.1350.
10
Experimental autoimmune encephalomyelitis induction in genetically B cell-deficient mice.在基因敲除B细胞的小鼠中诱导实验性自身免疫性脑脊髓炎
J Exp Med. 1996 Dec 1;184(6):2271-8. doi: 10.1084/jem.184.6.2271.