Special Issue "Combination of PD-1 and PD-1 Ligands in Immune Responses and Cancer Immunotherapies"

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Tumor Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (15 November 2018)

Special Issue Editors

Guest Editor
Dr. Yvette E. Latchman

NantCell Inc/Etubics Corportion, 410 West Harrison Street, Suite 200, Seattle, WA, USA
Website | E-Mail
Interests: coinhibitory pathways; vaccines; cancer immunotherapy; colorectal cancer; neoantigens
Guest Editor
Dr. Nadeem Sheikh

Dendreon, 1208 Eastlake Avenue East, Seattle, WA, USA
Website | E-Mail
Phone: 206 219 1015
Interests: cancer immunotherapy; biomarkers; vaccines; prostate cancer
Co-Guest Editor
Dr. Hong Tang

Dendreon, 1208 Eastlake Avenue East, Seattle, WA, USA
Interests: cancer immunotherapy, CAR T cells, checkpoint inhibitors, urology, prostate cancer

Special Issue Information

Dear Colleagues,

Checkpoint (co-inhibitory) pathways were originally defined by their ability to inhibit or dampen T cell mediated responses. Preclinical studies in tumor models and clinical trials demonstrated that blocking of the prototype inhibitory pathway, CTLA-4 and its ligands CD80 and CD86, lead to tumor regression primarily in melanoma. This resulted in the first FDA approved checkpoint inhibitor, Ipilimumab (YERVOY®), an antibody targeting CTLA-4. The discovery of PD-1 in the early 1990s and later its ligands PD-l, and PD-L2 was the first hint that there were additional members of the checkpoint family which were distinct in functionality from CTLA-4. The wide-ranging expression of PD-1 ligands in particular PD-L1 on non-immune cells pointed to the broad immunoregulatory role of the PD-1-PDL pathway in maintaining self-tolerance. In addition, the high expression of PD-1 on ‘exhausted’ T cells in the context of non-functional antigen-specific CD8+ T cells in anti-viral immunity and within the tumor microenvironment, together with expression of PD-L1 on tumors suggested the possibility that blocking the PD-1-PD-L1 axis would result in an enhanced anti-tumor response. Over the last decade, a plethora of studies including murine tumor models and clinical trials have demonstrated that PD-1 checkpoint inhibitors are capable of enhancing tumor immunity and could lead to subsequent tumor regression. At present, there are five FDA-approved PD-1/PDL1 checkpoint inhibitors, Pembrolizumab (Keytruda®) and nivolumab (Opdivo®) target the PD-1 receptor, and Atezolizumab (Tenectriq®, Avelumab (BAVENCIO®) and Durvalumab ((IMFINZI®) target PD-L1. Compared to the CTLA-4 checkpoint inhibitor, the number of cancer indications that can be treated with PD-1/PD-L1 checkpoint inhibitors have increased including, but not confined to, metastatic non-small cell lung cancer, classical Hodgkin lymphoma and mismatch-repair deficient (dMMR) metastatic colorectal cancer. Although PD-1:PD-L1 inhibitors have proven very successful in some patients, the majority of patients across  a broad range of indications show little or no response to the PD-1/PDL1 checkpoint inhibitors. Although combination of PD-1 and PD-1 ligands with CTLA-4 inhibitors is showing some improvement in the response rate in patients, there are still unanswered questions about which combination(s) will be the most efficacious and how restrictive these combinations will be to certain cancer types.

Therefore, the emphasis of this Special Issue “Combination of PD-1 and PD-1 Ligands in Immune Responses and Cancer Immunotherapies” will be on pre-clinical and clinical studies in various cancers addressing the following topics:

  • Combination of PD-1/PDL inhibitors with new co-inhibitory pathways.
  • Combination of PD-1/PDL inhibitors with various other treatment modalities including but not limited to vaccines, targeting immunosuppressive cells in the tumor environment and chemotherapy
  • Vaccines against Neoantigen in combination of PD-1/PDL inhibitors
  • Combination of PD-1/PDL inhibitors and targeting NK cells
  • Biomarkers other than PD-L1 that are associated with combination therapies and PD-1/PDL inhibitor responses.

Dr. Yvette E. Latchman
Dr. Nadeem Sheikh
Dr. Hong Tang
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 550 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • PDL1 checkpoint inhibitors and new coinhibitory pathways
  • PDL1 checkpoint inhibitors and vaccines
  • PDL1 checkpoint inhibitors and neoantigens
  • PDL1 checkpoint inhibitors and targeting immunosuppressive cells in tumor
  • PDL1 checkpoint inhibitors and NK cells
  • PDL1 checkpoint inhibitors and biomarkers

Published Papers (1 paper)

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Open AccessReview The Role of Yes-Associated Protein (YAP) in Regulating Programmed Death-Ligand 1 (PD-L1) in Thoracic Cancer
Biomedicines 2018, 6(4), 114; https://doi.org/10.3390/biomedicines6040114
Received: 10 November 2018 / Revised: 29 November 2018 / Accepted: 4 December 2018 / Published: 7 December 2018
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The programmed death-ligand 1(PD-L1)/PD-1 pathway is an immunological checkpoint in cancer cells. The binding of PD-L1 and PD-1 promotes T-cell tolerance and helps tumor cells escape from host immunity. Immunotherapy targeting the PD-L1/PD-1 axis has been developed as an anti-cancer therapy and used
[...] Read more.
The programmed death-ligand 1(PD-L1)/PD-1 pathway is an immunological checkpoint in cancer cells. The binding of PD-L1 and PD-1 promotes T-cell tolerance and helps tumor cells escape from host immunity. Immunotherapy targeting the PD-L1/PD-1 axis has been developed as an anti-cancer therapy and used in treating advanced human non-small cell lung cancer (NSCLC) and malignant pleural mesothelioma (MPM). Yes-associated protein (YAP) is a key mediator of the Hippo/YAP signaling pathway, and plays important roles in promoting cancer development, drug resistance and metastasis in human NSCLC and MPM. YAP has been suggested as a new therapeutic target in NSCLC and MPM. The role of YAP in regulating tumor immunity such as PD-L1 expression has just begun to be explored, and the correlation between YAP-induced tumorigenesis and host anti-tumor immune responses is not well known. Here, we review recent studies investigating the correlation between YAP and PD-L1 and demonstrating the mechanism by which YAP regulates PD-L1 expression in human NSCLC and MPM. Future work should focus on the interactions between Hippo/YAP signaling pathways and the immune checkpoint PD-L1/PD-1 pathway. The development of new synergistic drugs for immune checkpoint PD-L1/PD-1 blockade in NSCLC and MPM is warranted. Full article

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