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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
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Increased expression of PD‑L1 by the human papillomavirus 16 E7 oncoprotein inhibits anticancer immunity

Chaoqi Liu1, Jiao Lu1, Huiqun Tian1

  • 1Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, Hubei 443001, P.R. China.

Molecular Medicine Reports
|January 12, 2017
PubMed

Insights

Human papillomavirus (HPV) E7 protein drives cervical cancer immune evasion by increasing PD-L1 expression, leading to T cell dysfunction. Restoring T cell activity may involve inhibiting the PD-L1/PD-1 pathway.

Area of Science:

  • Immunology
  • Oncology
  • Virology

Background:

  • Cytotoxic T lymphocyte (CTL) dysfunction, often linked to PD-L1/PD-1 pathway activation, presents a major challenge in cancer therapy.
  • Human papillomavirus (HPV) infection is a primary cause of cervical cancer and can contribute to immune evasion.

Purpose of the Study:

  • To investigate the mechanisms by which HPV-induced cervical cancer cells evade the host immune system via the PD-L1/PD-1 signaling pathway.
  • To explore the potential of targeting the PD-L1/PD-1 pathway for cervical cancer immunotherapy.

Main Methods:

  • Comparative analysis of HPV16E7 and PD-L1 expression in cervical tissues using immunohistochemistry and RT-PCR.
  • In vitro studies involving overexpression and knockdown of HPV16E7 in cancer cell lines (PC3, CaSki).
  • Assessment of peripheral blood mononuclear cell (PBMC) proliferation and CTL activity.
  • Transfection of CaSki cells with a soluble PD-1 expressing plasmid and co-culture with PBMCs.

Main Results:

  • Significantly elevated HPV16E7 and PD-L1 expression in cervical cancer tissues compared to normal tissues, with a positive correlation between them.
  • Overexpression of HPV16E7 increased PD-L1 levels, inhibiting PBMC proliferation and CTL activity.
  • HPV16E7 knockdown reduced PD-L1 expression and enhanced PBMC proliferation and CTL activity.
  • Soluble PD-1 treatment significantly increased PBMC proliferation and CTL activity.

Conclusions:

  • HPV16E7-induced PD-L1 overexpression contributes to lymphocyte dysfunction in cervical cancer.
  • Inhibiting the PD-L1/PD-1 pathway, potentially with soluble PD-1, can restore tumor-infiltrating lymphocyte function.
  • These findings offer novel insights for developing immunotherapeutic strategies against cervical cancer.

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