Capture of target cell membrane components via trogocytosis is triggered by a selected set of surface molecules on T or B cells

被引:74
作者
Hudrisier, Denis
Aucher, Anne
Puaux, Anne-Laure
Bordier, Christine
Joly, Etienne
机构
[1] CNRS, Inst Pharmacol & Biol Struct, UMR 5089, F-31077 Toulouse 3, France
[2] Univ Toulouse 3, F-31062 Toulouse, France
关键词
D O I
10.4049/jimmunol.178.6.3637
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Key events of T and B cell biology are regulated through direct interaction with APC or target cells. Trogocytosis is a process whereby CD4(+) T, CD8(+) T, and B cells capture their specific membrane-bound Ag through the acquisition of plasma membrane fragments from their cellular targets. With the aim of investigating whether the ability to trigger trogocytosis was a selective property of Ag receptors, we set up an assay that allowed us to test the ability of many different cell surface molecules to trigger trogocytosis. On the basis of the analysis of a series of surface molecules on CD4(+) T, CD8(+) T, and B cells, we conclude that a set of cell type-specific surface determinants, including but not limited to Ag receptors, do trigger trogocytosis. On T cells, these determinants include components of the TCR/CD3 as well as that of coreceptors and of several costimulatory molecules. On B cells, we identified only the BCR and MHC molecules as potentials triggers of trogocytosis. Remarkably, latrunculin, which prevents actin polymerization, impaired trogocytosis by T cells, but not by B cells. This was true even when the same Abs were used to trigger trogocytosis in T or B cells. Altogether, our results indicate that although trogocytosis is performed by all hemopoietic cells tested thus far, both the receptors and the mechanisms involved can differ depending on the lineage of the cell acquiring membrane materials from other cells. This could therefore account for the different biological consequences of Ag capture via trogocytosis proposed for different types of cells.
引用
收藏
页码:3637 / 3647
页数:11
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