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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
|December 31, 2016
PubMed

Insights

Human papillomavirus (HPV) E7 protein drives cervical cancer immune evasion by increasing PD-L1 expression, leading to T cell dysfunction. Soluble PD-1 therapy may restore anti-tumor immunity by blocking this pathway.

Area of Science:

  • Immunology
  • Oncology
  • Virology

Background:

  • Cytotoxic T lymphocyte (CTL) dysfunction, often due to PD-L1/PD-1 pathway activation, hinders cancer therapy.
  • Human papillomavirus (HPV) infection is a major cause of cervical cancer.
  • Understanding HPV's role in immune evasion is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the mechanisms of HPV-induced immune evasion in cervical cancer via the PD-L1/PD-1 pathway.
  • To determine the correlation between HPV16E7 oncoprotein and PD-L1 expression.
  • To evaluate the potential of soluble PD-1 as an immunotherapeutic strategy.

Main Methods:

  • Immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR) to assess HPV16E7 and PD-L1 expression.
  • Overexpression and knockdown of HPV16E7 in cervical cancer cell lines (PC3, CaSki).
  • In vitro co-culture assays with peripheral blood mononuclear cells (PBMCs) and T cells.
  • Transfection with a soluble PD-1 expressing plasmid.

Main Results:

  • Increased HPV16E7 and PD-L1 expression in cervical cancer tissues compared to normal tissues.
  • HPV16E7 overexpression elevated 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.
  • Targeting the PD-L1/PD-1 pathway with soluble PD-1 may restore anti-tumor immune responses.
  • These findings offer novel insights for cervical cancer immunotherapy.

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