Presentation of antagonist peptides to naive CD4+ T cells abrogates spatial reorganization of class II MHC peptide complexes on the surface of dendritic cells
Presentation of antagonist peptides to naive CD4+ T cells abrogates spatial reorganization of class II MHC peptide complexes on the surface of dendritic cells
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DOI：
10.1073/pnas.222463499
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发表时间：
2002-11-12
影响因子：
11.1
通讯作者：
Ignatowicz, L
中科院分区：
文献类型：
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作者：
Chmielowski, B;Pacholczyk, R;Ignatowicz, L
通过使用逆转录病毒转导的树突状细胞(DC)，编码带有荧光蛋白的共价A(B)β/肽融合蛋白，我们跟踪了在初始和效应CD4(+)T细胞开始激活的过程中，携带激动剂或零肽的II类MHC分子的重新定位。树突状细胞表面形成T细胞受体(TCR)/CD3复合体和II类激动剂MHC/肽复合体。然而，幼稚但不是效应性T细胞的激活伴随着从T细胞-DC界面排出的空的II类MHC/肽复合体。这些效应在外源提供的拮抗肽的存在下被干扰。这些结果表明，干扰激动剂和无效MHC/肽复合体在免疫突触中的选择性重新定位，可能是拮抗肽抑制初始的CD4(+)T细胞对激动剂配体的反应的原因之一。
By using dendritic cells (DCs) transduced with retroviruses encoding covalent A(b)beta/peptide fusion proteins tagged with fluorescent proteins, we followed the relocation of class II MHC molecules loaded with agonist or null peptides during the onset of activation of naive and effector CD4(+) T cells. Clusters of T cell receptor (TCR)/CD3 complex formed in parallel with clusters of agonist class II MHC/peptide complexes on the surface of DCs. However, activation of naive but not effector T cells was accompanied by expulsion of the null class II MHC/peptide complexes from the T cell-DC interface. These effects were perturbed in the presence of exogenously supplied antagonist peptide. These results suggest that interference with selective relocation of agonist and null MHC/peptide complexes in the immunological synapse contributes to the inhibitory effect of antagonist peptides on the response of naive CD4(+) T cells to agonist ligands.