Interaction of CD2 with its ligand, LFA-3, in human T cell proliferation.

Interaction of CD2 with its ligand, LFA-3, in human T cell proliferation.
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DOI:
10.4049/jimmunol.140.10.3358
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发表时间:
1988-05
影响因子:
4.4
通讯作者:
B. Bierer;J. Barbosa;S. Herrmann;S. Burakoff
B. Bierer;J. Barbosa;S. Herrmann;S. Burakoff
中科院分区:
医学2区
文献类型:
--
作者:
B. Bierer;J. Barbosa;S. Herrmann;S. Burakoff

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最近的研究表明,淋巴细胞功能相关抗原(LFA-3)是CD2的天然配体,这种受体-配体相互作用在细胞间的黏附中起作用。在这份报告中,我们证明了LFA-3在T细胞激活中发挥作用。将人基因组DNA导入L细胞,筛选LFA-3的表达。我们证明LfA-3+L细胞与抗CD3mAb或亚适量的PHA共同刺激人外周血T细胞的增殖。此外,LFA-3+L细胞和次适剂量的PHA均可诱导胸腺细胞增殖。针对CD2或LFA-3的mAb均可抑制细胞增殖。用PHA和LFA-3+L细胞联合刺激胸腺细胞后,IL-2R以及表面抗原4F2、转铁蛋白受体和人类白细胞抗原-DR的表达增加。这些数据支持LFA-3在CD2依赖的T细胞活化中发挥作用的结论。LFA-3分布广泛,在APC和靶细胞上均有表达。因此,CD2/LFA-3相互作用与抗CD3单抗协同刺激的能力表明,CD2/LFA-3相互作用不仅可能参与非抗原依赖的T细胞激活的替代途径,而且还参与抗原特异性T细胞的激活。
Recently, it has been demonstrated that lymphocyte function-associated Ag (LFA-3) is a natural ligand for CD2 and that this receptor-ligand interaction functions in cell-cell adhesion. In this report, we demonstrate that LFA-3 plays a role in T cell activation. L cells were transfected with human genomic DNA and sorted for expression of LFA-3. We demonstrate that LFA-3+ L cells, together with anti-CD3 mAb or with suboptimal doses of PHA, stimulate proliferation of human peripheral blood T cells. Furthermore, thymocyte proliferation was induced by LFA-3+ L cells and suboptimal doses of PHA. Proliferation was inhibited by mAb directed against either CD2 or LFA-3. Stimulation of thymocytes by the combination of PHA and LFA-3+ L cells resulted in the increased expression of the IL-2R, as well as of the surface Ag 4F2, transferrin receptor, and HLA-DR. These data support the conclusion that LFA-3 plays a role in CD2-dependent T cell activation. LFA-3 is widely distributed and is expressed on all APC and target cells. Thus, the ability of the CD2/LFA-3 interaction to costimulate with an anti-CD3 mAb suggests that the CD2/LFA-3 interaction may be involved not only in an Ag-independent alternate pathway of T cell activation but also in Ag-specific T cell activation.