The roles of programmed death ligand 1 in virus-associated cancers
Morvarid Golrokh Mofrad1, Donya Taghizadeh Maleki2, Ebrahim Faghihloo2
1Human Viral Vaccine Department, Razi Vaccine & Serum Research Institute, Agricultural Research, Education & Extension Organization (AREEO), Karaj, Iran.
Abstract:
Programmed death ligand 1 (PD-L1) is a surface glycoprotein that induces T-cell anergy or apoptosis by binding to PD-1 on activated T and B cells. It is also known as a cluster of differentiation 274 (CD274) or B7 homolog 1 (B7-H1). Suppressing the adaptive arm of the immune system is the critical role of PD-L1.so it prohibits the proliferation of activated T cells and reduces apoptosis in regulatory T cells. When PD-L1 binds to PD-1, it prevents T cells from killing other cells such as cancer cells. Viruses have various strategies to evade from the immune system such as modifying host gene expression or deregulating proteins function. So they can directly or indirectly change the expression of PD-L1. This study proposed to evaluate the effect of viruses on the expression of PD-L1 which leading to uncontrolled cell growth and tumor formation. We have studied serious tumorigenic viruses, including Human Papillomaviruses (HPV), Epstein-Barr viruses (EBV), Human T-cell leukemia viruses type 1 (HTLV-1), Hepatitis B viruses (HBV) and Hepatitis C viruses (HCV). So we surveyed the correlation between the presence of viruses and expression of PD-L1. Most studies showed the PD-L1 overexpression due to viral functions; however, further studies are needed to better understand the role of the PD-1/PD-L1 pathway in virus-associated cancers as a candidate of anti- PD-L1 therapy.
Insights
Viruses can alter the expression of programmed death ligand 1 (PD-L1), a key immune checkpoint. This viral manipulation of PD-L1 may contribute to uncontrolled cell growth and tumor formation in virus-associated cancers.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- Programmed death ligand 1 (PD-L1), also known as CD274 or B7-H1, is a surface glycoprotein that suppresses T-cell responses.
- PD-L1 binding to PD-1 inhibits T-cell proliferation and promotes regulatory T-cell survival, thereby hindering the immune system's ability to eliminate cancer cells.
- Viruses employ diverse strategies to evade immune surveillance, including modulation of host gene expression and protein function, which can impact PD-L1 levels.
Purpose of the Study:
- To investigate the effect of various tumorigenic viruses on the expression of PD-L1.
- To evaluate the correlation between viral presence and PD-L1 expression.
- To explore the potential of the PD-1/PD-L1 pathway as a therapeutic target in virus-associated cancers.
Main Methods:
- Literature review and survey of existing studies.
- Analysis of the association between specific viruses and PD-L1 expression.
- Identification of tumorigenic viruses including HPV, EBV, HTLV-1, HBV, and HCV.
Main Results:
- Most studies indicate that viral infections lead to the overexpression of PD-L1.
- Viral functions appear to be a significant factor in the upregulation of PD-L1.
- A correlation between the presence of certain viruses and elevated PD-L1 expression was observed.
Conclusions:
- Viral infections can significantly influence PD-L1 expression, potentially contributing to tumor development.
- The PD-1/PD-L1 pathway is implicated in the pathogenesis of virus-associated cancers.
- Further research is warranted to fully elucidate the role of PD-1/PD-L1 in these cancers and its potential for anti-PD-L1 therapies.
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