Ionizing Radiation Reduces Head and Neck Squamous Cell Carcinoma Cell Viability and Is Associated with Predictive Tumor-Specific T Cell Responses

Author:

Upadhaya Puja1,Ryan Nathan1ORCID,Roth Peyton1,Pero Travis2,Lamenza Felipe13,Springer Anna1,Jordanides Pete1,Pracha Hasan1,Mitchell Darrion4ORCID,Oghumu Steve1ORCID

Affiliation:

1. Department of Pathology, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA

2. College of Dentistry, The Ohio State University, Columbus, OH 43210, USA

3. Department of Microbiology, The Ohio State University, Columbus, OH 43210, USA

4. Department of Radiation Oncology, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA

Abstract

Head and neck squamous cell carcinoma (HNSCC) is common and deadly, and there is a need for improved strategies to predict treatment responses. Ionizing radiation (IR) has been demonstrated to improve HNSCC outcomes, but its effects on immune responses are not well characterized. We determined the impact of IR on T cell immune responses ex vivo. Human and mouse HNSCC cells were exposed to IR ranging from 20 to 200 Gy to determine cell viability and the ability to stimulate T-cell-specific responses. Lymph node cells of LY2 and MOC2 tumor-bearing or non-tumor-bearing mice were re-stimulated with a tumor antigen derived from LY2 or MOC2 cells treated with 200 Gy IR, ultraviolet (UV) exposure, or freeze/thaw cycle treatments. T cell proliferation and cytokine production were compared to T cells restimulated with plate-bound CD3 and CD28 antibodies. Human and mouse HNSCC cells showed reduced viability in response to ionizing radiation in a dose-dependent manner, and induced expression of T cell chemotactic cytokines. Tumor antigens derived from IR-treated LY2 and MOC2 cells induced greater proliferation of lymph node cells from tumor-bearing mice and induced unique T cell cytokine expression profiles. Our results demonstrate that IR induces potent tumoral immune responses, and IR-generated tumor antigens can potentially serve as an indicator of antitumor immune responses to HNSCC in ex vivo T cell restimulation assays.

Funder

National Cancer Institute

National Institute of Dental and Craniofacial Research

American Cancer Society

Publisher

MDPI AG

Subject

Cancer Research,Oncology

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