EFFECT OF HYPERTONICITY AND MONENSIN ON CD3/TCR SURFACE EXPRESSION IN HUMAN T-CELLS
EFFECT OF HYPERTONICITY AND MONENSIN ON CD3/TCR SURFACE EXPRESSION IN HUMAN T-CELLS
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DOI：
10.1016/0165-2478(88)90129-0
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发表时间：
1988-10-01
影响因子：
4.4
通讯作者：
FEHLMANN, M
中科院分区：
文献类型：
--
作者：
DALLANEGRA, A;SCHAFFAR, L;FEHLMANN, M
用抗CD3或抗TCR单抗预处理T淋巴细胞可导致T细胞受体复合物（TCR/CD3）从细胞表面消失。这种下调的机制尚未完全阐明。我们在这里证明了CD3/TCR复合物的调节可以被高渗介质完全抑制，这种情况已知会阻断受体介导的内吞作用。因此，在高渗条件下，酸性囊泡中与相关单抗相关的CD3/TCR复合物的隔离并未发生。此外，已知干扰受体循环的莫能菌素被发现可以放大特异性单抗诱导的CD3/TCR调节，并减少T细胞对125i标记的antid3 /TCR单抗的摄取。因此，我们提出单克隆抗体- cd3 /TCR复合物通过受体介导的内吞作用通过涂层凹坑内化，然后转运到酸室。在此过程中，单抗在溶酶体中被降解，而CD3/TCR分子则循环回到细胞表面。
Pretreatment of T lymphocytes with anti-CD3 or anti-TCR mAb results in the disappearance of the T cell receptor complex (TCR/CD3) from the cell surface. The mechanisms of this down-regulation have not been fully elucidated. We demonstrate here that the modulation of the CD3/TCR complex can be completely inhibited by hypertonic medium, a condition known to block receptor-mediated endocytosis. Consequently, the sequestration of the CD3/TCR complex associated to relevant mAB in acid vesicles did not occur under hypertonicity condition. Moreover, monensin, which is known to interfere with receptor recycling, was found to amplify the CD3/TCR modulation induced by specific mAb and decrease the uptake of 125I-labeled antiCD3/TCR mAb by T cells. We therefore propose that mAb-CD3/TCR complexes are internalized via coated pits by a receptor-mediated endocytosis and then transported to acid compartments. MAb are degraded in lysosomes during this process, whereas CD3/TCR molecules recycle back to cell surface.