| Literature DB >> 28919987 |
Salvinia Mletzko1, David J Pinato1, Rebecca C Robey1, Alessia Dalla Pria2, Peter Benson3, Nesrina Imami1, Mark Bower1,2.
Abstract
Upregulation of programmed death ligand 1 (PD-L1) is a mechanism of immune escape utilized by a variety of tumors. PD-L1 expression in tumor cells or in the surrounding infiltrate correlates with clinical responsiveness to novel therapies targeting the PD-1/PD-L1 immune checkpoint. In the context of HIV-1 infection, Kaposi's sarcoma (KS) is largely responsive to restoration of immunity following combination antiretroviral therapy (cART), but there is a subset that is not. We hypothesized that this subset of cART-refractory KS may utilize the PD-L1 pathway of immune escape. We found that PD-L1 expressing KS had a denser CD8+ T cell (p = 0.03) and PD-L1 positive macrophage peritumoral infiltrate (p = 0.04) to suggest the involvement of PD-L1 in shaping an immune-tolerogenic microenvironment in cART-refractory KS. The presence of PD-L1 expression in association with immune-infiltrating cells provides rationale for the clinical development PD-1/PD-L1-targeted checkpoint inhibitors in cART-refractory KS.Entities:
Keywords: HIV; KS; PD-L1; cART; microenvironment
Year: 2017 PMID: 28919987 PMCID: PMC5593697 DOI: 10.1080/2162402X.2017.1304337
Source DB: PubMed Journal: Oncoimmunology ISSN: 2162-4011 Impact factor: 8.110