Accumulation of MHC class II+ CD11c- non-lymphoid cells in the spleen during infection with Plasmodium yoelii is lymphocyte-dependent.
Accumulation of MHC class II+ CD11c- non-lymphoid cells in the spleen during infection with Plasmodium yoelii is lymphocyte-dependent.
复制标题
约氏疟原虫感染期间，脾脏中 MHC II 类 CD11c-非淋巴细胞的积累是淋巴细胞依赖性的。
DOI：
10.1111/1348-0421.12024
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发表时间：
2013
影响因子：
2.6
通讯作者：
Yui K,
中科院分区：
文献类型：
--
作者：
Kamei R;Miyakoda M;Tamura T;Kimura D;Honma K;Kimura K;Yui K,
脾脏是疟原虫感染时免疫防御的主要器官，脾肿大是疟原虫感染的主要症状之一。使用约氏疟原虫感染的啮齿动物模型，表征了脾脏中的MHC II类+CD 11 c −非T、非B细胞。虽然传统树突状细胞的比例减少，但在感染过程中，MHC II+ CD 11 c −非T、非B细胞的比例增加。该亚群的增加依赖于淋巴细胞的存在。使用过继转移正常脾细胞的Rag-2−/−小鼠进行的实验表明，这些细胞是非淋巴细胞;然而，在感染P. yoeliidependedonlymphocytes.在功能上，这些MHC II+ CD 11 c −非T、非B细胞能够产生促炎细胞因子α肿瘤坏死因子和白细胞介素6，以响应感染的红细胞，但激活抗原特异性CD 4 +T细胞的能力有限。这项研究揭示了一种新的MHC II+ CD 11 c −非淋巴细胞和淋巴细胞之间的相互作用，这些非淋巴细胞在感染P. yoelii。
The spleen is the main organ for immune defense during infection withPlasmodiumparasites and splenomegaly is one of the major symptoms of such infections. Using a rodent model ofPlasmodium yoeliiinfection, MHC class II+CD11c−non‐T, non‐B cells in the spleen were characterized. Although the proportion of conventional dendritic cells was reduced, that of MHC II+CD11c−non‐T, non‐B cells increased during the course of infection. The increase in this subpopulation was dependent on the presence of lymphocytes. Experiments using Rag‐2−/−mice with adoptively transferred normal spleen cells indicated that these cells were non‐lymphoid cells; however, their accumulation in the spleen during infection withP. yoeliidepended on lymphocytes. Functionally, these MHC II+CD11c−non‐T, non‐B cells were able to produce the proinflammatory cytokines alpha tumor necrosis factor and interleukin‐6 in response to infected red blood cells, but had only a limited ability to activate antigen‐specific CD4+T cells. This study revealed a novel interaction between MHC II+CD11c−non‐lymphoid cells and lymphoid cells in the accumulations of these non‐lymphoid cells in the spleen during infection withP. yoelii.