Bcl6 is essential for the generation of long-term memory CD4+ T cells
Bcl6 is essential for the generation of long-term memory CD4+ T cells
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DOI：
10.1093/intimm/dxm007
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发表时间：
2007-04-01
影响因子：
4.4
通讯作者：
Tokuhisa, Takeshi
中科院分区：
文献类型：
--
作者：
Ichii, Hirohito;Sakamoto, Akemi;Tokuhisa, Takeshi
Bcl6在记忆性CD8(+)T细胞的产生和维持中起作用。我们在这里分析了Bcl6在产生长期记忆的CD4(+)T细胞中的作用。将Bcl6基因缺陷的DO11.10(KJ1.26(+))转基因小鼠的CD45RB(+)CD4(+)T细胞转移到BALB/c小鼠体内，用卵白蛋白多肽和脂多糖免疫小鼠。免疫后10周，在脾、肺、肝等脏器中检测到野生型小鼠的长期记忆KJ1.26(+)CD4(+)T细胞，而在免疫后4周，这些器官中Bcl6缺失的KJ1.26(+)CD4(+)T细胞完全消失。由于Bcl6缺陷的效应细胞可产生记忆性的CD4(+)T细胞，因此在免疫后10天比较了Bcl6缺陷的效应细胞和野生型效应细胞的特性。脾、肺、肝中不产生干扰素-γ的CD45RB(-)、CD62L(+)或IL-7Rα(+)效应T细胞在Bcl6缺陷型和野生型CD4(+)T细胞中的数量相似。然而，Bcl6缺陷的效应型CD4(+)T细胞的凋亡率高于野生型效应型CD4(+)T细胞。在效应后期，Bcl6缺陷的CD4(+)T细胞的干扰素非产生细胞数低于野生型，而凋亡率高于野生型。这些结果提示，Bcl6在CD4(+)T细胞中具有保护记忆前体细胞的作用，可能与长期记忆的CD4(+)T细胞的存活有关。
Bcl6 plays a role in the generation and maintenance of memory CD8(+) T cells. We analyzed here a role for Bcl6 in the generation of long-term memory CD4(+) T cells. Naive CD45RB(+) CD4(+) T cells from Bcl6-deficient DO11.10 (KJ1.26(+)) transgenic mice were transferred into BALB/c mice and immunized with ovalbumin peptide and LPS. Long-term memory KJ1.26(+) CD4(+) T cells from wild-type mice were detected in the spleen, lungs and liver during 10 weeks after immunization; however, Bcl6-deficient KJ1.26(+) CD4(+) T cells were vanished completely in those organs 4 weeks after immunization. Since memory CD4(+) T cells can be generated from effector CD4(+) T cells, properties of Bcl6-deficient effector CD4(+) T cells were compared with those wild-type effector CD4(+) T cells 10 days after immunization. Numbers of IFN-gamma-non-producing CD45RB(-), CD62L(+) or IL-7R alpha(+) effector CD4(+) T cells in the spleen, lungs and liver were similar between Bcl6-deficient and wild-type CD4(+) T cells. However, the percentage of apoptotic cells in Bcl6-deficient effector CD4(+) T cells was higher than that in wild-type effector CD4(+) T cells. At the late effector phase, the number of IFN-gamma-non-producing cells and the percentage of apoptotic cells in Bcl6-deficient CD4(+) T cells were smaller and higher than those in wild-type CD4(+) T cells, respectively. These data suggest that Bcl6 in CD4(+) T cells plays a role in protection of memory precursor CD4(+) T cells from apoptosis and may involve in survivability of long-term memory CD4(+) T cells.