Malaria infection changes the ability of splenic dendritic cell populations to stimulate antigen-specific T cells.
Malaria infection changes the ability of splenic dendritic cell populations to stimulate antigen-specific T cells.
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疟疾感染改变了脾树突状细胞群体刺激抗原特异性T细胞的能力。
DOI：
10.1084/jem.20052450
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发表时间：
2006-06-12
影响因子：
15.3
通讯作者：
Langhorne, Jean
中科院分区：
文献类型：
--
作者：
Sponaas, Anne-Marit;Cadman, Emma Tamsin;Voisine, Cecile;Harrison, Vicky;Boonstra, Andre;O' Garra, Anne;Langhorne, Jean
小鼠夏氏疟原虫感染期间脾脏CD 11 c+树突状细胞（DC）群体向T细胞呈递抗原（Ag）的能力不同。在感染过程中，CD 11 c + CD 8+和CD 8 − DCs都在其表面呈递疟疾肽。然而，尽管表达疟疾肽的两种DC亚群都可以诱导CD 4 T细胞产生干扰素-γ，但只有在感染急性期分离的CD 8 − DC刺激Ag特异性T细胞增殖，并刺激Ag转基因T细胞从MSP 1特异性T细胞受体产生白细胞介素（IL）-4和IL-10，这与我们报道的在此阶段响应病原体的Th 1向Th 2转换相一致。这些不同的DC反应的时间与CD 8+群体中凋亡水平的增加和脾脏中CD 8 − DC数量的增加相一致。我们的数据表明，在夏氏疟原虫感染的小鼠中观察到的CD 4 T细胞应答的转换可能是由疟疾感染修饰的不同DC群体呈递的结果。
The capacity of splenic CD11c+ dendritic cell (DC) populations to present antigen (Ag) to T cells differs during malarial infection with Plasmodium chabaudi in mice. Both CD11c+CD8+ and CD8− DCs presented malarial peptides on their surface during infection. However, although both DC subsets expressing malaria peptides could induce interferon-γ production by CD4 T cells, only CD8− DCs isolated at the acute phase of infection stimulated Ag-specific T cell proliferation and interleukin (IL)-4 and -10 production from MSP1-specific T cell receptor for Ag transgenic T cells coincidental with our reported Th1 to Th2 switch at this stage in response to the pathogen. The timing of these distinct DC responses coincided with increased levels of apoptosis in the CD8+ population and an increase in the numbers of CD8− DCs in the spleen. Our data suggest that the switch in CD4 T cell responses observed in P. chabaudi–infected mice may be the result of the presentation by different DC populations modified by the malaria infection.
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Toll样受体9介导疟疾色素血液唑素的先天免疫激活。
DOI：
10.1084/jem.20041836
发表时间：
2005-01-03
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Coban C;Ishii KJ;Kawai T;Hemmi H;Sato S;Uematsu S;Yamamoto M;Takeuchi O;Itagaki S;Kumar N;Horii T;Akira S
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影响因子：
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通讯作者：
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影响因子：
32.4
作者：
Jung, S;Unutmaz, D;Lang, RA
通讯作者：
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影响因子：
3.1
作者：
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通讯作者：
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影响因子：
32.4
作者：
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