Differential requirements for antigen or homeostatic cytokines for proliferation and differentiation of human Vγ9Vδ2 naive, memory and effector T cell subsets
Differential requirements for antigen or homeostatic cytokines for proliferation and differentiation of human Vγ9Vδ2 naive, memory and effector T cell subsets
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DOI：
10.1002/eji.200525983
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发表时间：
2005-06-01
影响因子：
5.4
通讯作者：
Salerno, A
中科院分区：
文献类型：
--
作者：
Caccamo, N;Meraviglia, S;Salerno, A
我们比较了V γ 9V δ 2 T细胞的四个人亚群，幼稚T细胞，（T细胞初治，CD 45 RA（+）CD 27（+）），中枢记忆（T-CM，CD 45 RA（-）CD 27（+）），效应记忆（T-EM，CD 45 RA（-）CD 27（-））和终末分化（T-EMRA，CD 45 RA（+）CD 27（-）），因为它们响应于抗原或稳态细胞因子而增殖和分化的能力。细胞因子反应性和IL-15 R表达在T幼稚细胞中较低，并且从T-CM到T-EM和T-EMRA细胞逐渐增加。相反，在抗原或细胞因子刺激反应的能力，扩大显示出一个相互的模式，并与细胞死亡和Bcl-2表达的阻力。尽管抗原刺激的细胞获得T-CM或T-EM表型，IL-15刺激的细胞保持其表型，但T-CM细胞除外，其以各种组合表达CD 27和CD 45 RA。这些结果与离体溴脱氧尿苷掺入实验一起显示，人V γ 9V δ 2记忆T细胞在体外和体内具有不同的增殖和分化潜能，并且T-EMRA细胞在不存在抗原的情况下在稳态增殖后从T-CM亚群产生。
We have compared four human subsets of V gamma 9V delta 2 T cells, naive (T-naive, CD45RA(+)CD27(+)), central memory (T-CM, CD45RA(-)CD27(+)), effector memory (T-EM, CD45RA(-)CD27(-)) and terminally differentiated (T-EMRA, CD45RA(+)CD27(-)), for their capacity to proliferate and differentiate in response to antigen or homeostatic cytokines. Cytokine responsiveness and IL-15R expression were low in T-naive cells and progressively increased from T-CM to T-EM and T-EMRA cells. In contrast, the capacity to expand in response to antigen or cytokine stimulation showed a reciprocal pattern and was associated with resistance to cell death and Bcl-2 expression. Whereas antigen-stimulated cells acquired a T-CM or T-EM phenotype, IL-15-stimulated cells maintained their phenotype, with the exception of T-CM cells, which expressed CD27 and CD45RA in various combinations. These results, together with ex vivo bromodeoxyuridine incorporation experiments, show that human V gamma 9V delta 2 memory T cells have different proliferation and differentiation potentials in vitro and in vivo and that T-EMRA cells are generated from the T-CM subset upon homeostatic proliferation in the absence of antigen.