Functional and phenotypic analysis of human memory CD8+ T cells expressing CXCR3

Functional and phenotypic analysis of human memory CD8+ T cells expressing CXCR3
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DOI:
10.1189/jlb.1205725
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发表时间:
2006-08-01
影响因子:
5.5
通讯作者:
Takiguchi, Masafumi
Takiguchi, Masafumi
中科院分区:
医学3区
文献类型:
--
作者:
Kobayashi, Naoki;Kondo, Takaaki;Takiguchi, Masafumi

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几种趋化因子受体在幼稚T细胞、记忆T细胞和效应T细胞的迁移中起着重要作用。流式细胞仪分析显示,具有幼稚(CD27(+)CD28(+)CD45RA(+))或记忆型(CD27(+)CD28(+/-)CD45RA(+))表型的人CD8(+)T细胞包括高表达CXC趋化因子受体3(CXCR3(高))和低表达CXCR3(低)的人群,而具有效应表型(CD27(-)CD28(-)CD45RA(+/-))的人包括不表达CXCR3(CXCR3(-))和CXCR3(低)的人群。CXCR3的表达水平与记忆/效应表型之间的关系也适用于Epstein-Barr病毒或人类巨细胞病毒特异性CD8(+)T细胞。CD8(+)T细胞的CC趋化因子受体7(CCR7)(+)、CCR5(-)和CCR7(-)CCR5(-)亚群主要表达CXCR3(高)细胞,具有CD27(+)CD28(+)CD45RA(-)记忆表型,提示它们是中等分化的记忆细胞。事实上,CXCR3(高)CD27(+)CD28(+)CD45RA(-)-CD8(+)T细胞具有产生白细胞介素2和干扰素-γ的能力。这些结果表明,CXCR3在中等分化的记忆CD8(+)T细胞上表达上调。CXCR3(高)CD8(+)T细胞对CXCR3配体的迁移能力强于CXCR3(低)T细胞。由于CXCR3(高)记忆性CD8(+)T细胞不表达CCR5,CXCR3在这些记忆性CD8+T细胞上的高表达可能在这些细胞向炎症部位的迁移和分化中起重要作用。J.Leukoc。比奥尔。80:320-329;2006。
Several chemokine receptors play an important role in the migration of naive, memory, and effector T cells. Flow cytometric analyses showed that human CD8(+) T cells with naive (CD27(+)CD28(+)CD45RA(+)) or memory (CD27(+)CD28(+/-) CD45RA(+)) phenotypes included a population expressing a high level of CXC chemokine receptor 3 (CXCR3(high)) and one expressing a low level of it (CXCR3(low)), but those with the effector phenotype (CD27(-)CD28(-)CD45RA(+/-)) included a population that did not express CXCR3 (CXCR3(-)) and a CXCR3(low) population. This relation between the expression level of CXCR3 and memory/effector phenotypes also applied to Epstein-Barr virus- or human cytomegalovirusspecific CD8(+) T cells. CXCR3(high) cells were found predominantly in CC chemokine receptor 7 (CCR7)(+)CCR5(-) and CCR7(-)CCR5(-) subsets of CD8(+) T cells with the CD27(+)CD28(+)CD45RA(-) memory phenotype, suggesting that they are memory cells with intermediate differentiation. Indeed, CXCR3(high) CD27(+)CD28(+)CD45RA(-)-CD8(+) T cells had the ability to produce interleukin-2 and interferon-gamma. These results together indicate that the expression of CXCR3 is upregulated on intermediately differentiated memory CD8(+) T cells. CXCR3(high) CD8(+) T cells had a greater ability to migrate in response to CXCR3 ligands than CXCR3(low) ones. As CXCR3(high) memory CD8(+) T cells do not express CCR5, high expression of CXCR3 on these memory CD8+ T cells might play an important role in the migration of these cells to inflammatory sites and in their differentiation. J. Leukoc. Biol. 80: 320-329;2006.