Phenotypic characterization of human peripheral γδT-cell subsets in glioblastoma.

The antitumoral contribution of γδT cells depends on their activation and differentiation into effectors. This depends on different molecules and membrane receptors, which conditions their physiology. This study aimed to determine the phenotypic characteristics of γδT cells in glioblastoma (GBM) according to five layers of membrane receptors. Among ten GBM cases initially enrolled, five of them who had been confirmed by pathological examination and ten healthy controls underwent phenotyping of peripheral γδT cells by flow cytometry, using the following staining: αβTCR, γδTCR, CD3, CD4, CD8, CD16, CD25, CD27, CD28, CD45, CD45RA, CD56, NKG2D, CD272(BTLA), and CD279(PD-1). Compared with the controls, the results showed no significant change in the number of γδT cells. However, there was a decrease of double-negative (CD4 CD8 ) Tγδ cells and an increase of naive γδT cells, a lack of CD25 expression, a decrease of the expression of CD279, and a remarkable, but not significant, increase in the expression of the CD27 and CD28 costimulation markers. Among the γδT cell subsets, the number of Vδ2 decreased in glioblastoma and showed no significant difference in the expression of CD16, CD56, and NKG2D. In contrast, the number of Vδ1 increased in glioblastoma with overexpression of CD16, CD56, and NKG2D. Our results showed that γδT cells are prone to adopt a pro-inflammatory profile in the glioblastoma context, which suggests that they might be a potential tool to consider in T cell-based immunotherapy in glioblastoma. However, this requires additional investigation on a larger sample size.