Preferential accumulation of antigen-specific effector CD4 T cells at an antigen injection site involves CD62E-dependent migration but not local proliferation.

Preferential accumulation of antigen-specific effector CD4 T cells at an antigen injection site involves CD62E-dependent migration but not local proliferation.
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DOI:
10.1084/jem.20021690
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发表时间:
2003-03-17
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Jenkins MK
Jenkins MK
中科院分区:
其他
文献类型:
--
作者:
Reinhardt RL;Bullard DC;Weaver CT;Jenkins MK

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抗原特异性T细胞向非淋巴组织的迁移被认为对于从体内消除外来抗原是重要的。然而,最近的结果表明,活化的T细胞迁移到许多非淋巴组织提出了抗原特异性T细胞不迁移优先含有抗原的非淋巴组织的可能性。我们通过在局部皮下抗原注射后追踪全身的抗原特异性CD4 T细胞来解决这个问题。抗原特异性CD4 T细胞在皮肤引流淋巴结中增殖,并且经历最多细胞分裂的细胞获得与CD62 P结合的能力。随着时间的推移,具有产生干扰素γ潜力的CD62P结合抗原特异性CD4 T细胞优先在抗原注射部位聚集,但仅在表达CD62E的受体中聚集。令人惊讶的是,这些T细胞在注射部位没有增殖,尽管显示出比引流淋巴结中的T细胞更多的细胞分裂的证据。结果表明,最分裂的效应CD4 T细胞从淋巴结进入位点的抗原沉积通过识别CD62 E血管和保留在那里通过识别肽主要组织相容性复合体II分子的非增殖状态。
The migration of antigen-specific T cells to nonlymphoid tissues is thought to be important for the elimination of foreign antigens from the body. However, recent results showing the migration of activated T cells into many nonlymphoid tissues raised the possibility that antigen-specific T cells do not migrate preferentially to nonlymphoid tissues containing antigen. We addressed this question by tracking antigen-specific CD4 T cells in the whole body after a localized subcutaneous antigen injection. Antigen-specific CD4 T cells proliferated in the skin-draining lymph nodes and the cells that underwent the most cell divisions acquired the ability to bind to CD62P. As time passed, CD62P-binding antigen-specific CD4 T cells with interferon γ production potential accumulated preferentially at the site of antigen injection but only in recipients that expressed CD62E. Surprisingly, these T cells did not proliferate in the injection site despite showing evidence of more cell divisions than the T cells in the draining lymph nodes. The results suggest that the most divided effector CD4 T cells from the lymph nodes enter the site of antigen deposition via recognition of CD62E on blood vessels and are retained there in a nonproliferative state via recognition of peptide–major histocompatibility complex II molecules.
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