T cells are pivotal in combating cancer
however, they can become exhausted during tumour progression, losing their cytotoxic capacity and upregulating inhibitory receptors including PD-1 and TIGIT. While checkpoint blockade has emerged as a potent treatment option for numerous cancers, patient selection, long-term efficacy, and adverse effects still remain an issue. For these reasons, it is important to investigate other pathways that might lead to selective reactivation of the immune system. Co-stimulatory TNFRSF receptors, including 4-1BB and OX-40, have emerged as promising targets for reactivating exhausted T cells. However, their expression on exhausted peripheral and tumour-infiltrating lymphocytes (TILs) is not well characterised, particularly in cervical cancer (CC), which remains the leading cause of gynaecological cancer mortality in low- and middle-income countries. To investigate the expression of these receptors, PBMCs were collected from CC patients and healthy donors, along with TILs from tumour biopsies, and analysed using multiparametric flow cytometry. Our findings revealed an increased population of phenotypically exhausted (PD-1