Propensity to develop cervical cancer (CC) in human papilloma virus (HPV) infected individual could potentially involve the impaired immune functioning. Several stages of HPV surveillance by immune cells in tumor micro-environment (TME) is regulated mainly by transforming growth factor-beta (TGF-β) and is crucial for the establishment of CC. The role of TGF-β in the initiation and progression of CC is very complex and involve different suppressor of mothers against decapentaplegic homolog (SMAD) dependent and SMAD independent signaling mechanism(s). This review summarizes the handling of HPV by immune cells such as T lymphocytes, B lymphocytes, natural killer cells (NK), dendritic cells (DC), monocytes, macrophages, myeloid derived suppressor cells (MDSC) and their regulation by TGF-β. The hijack mechanisms adapted by HPV to evade this surveillance process is discussed. Biomarkers indicating the stages of CC and immune checkpoints that can be targeted for improved outcome are included for immune-based theragnostics. This review also addresses the direct actions of TGF-β on CC cells and tumor/immune cell interactions. Therapies focused on targeting TGF-β using small molecule inhibitors, monoclonal antibodies and TGF-β chimeric antigen receptor (CAR)T cells are collated to understand the current strategies related to TGF-β in the management of CC.
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| http://dx.doi.org/10.1016/j.intimp.2024.112837 | DOI Listing |
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