PD‐L1 and PD‐1 Expression in Thyroid Follicular Epithelial Dysplasia : Hashimoto Thyroiditis Related Atypia and Potential Papillary Carcinoma Precursor
Pakkanen, E., Kalfert, D., Ahtiainen, M., Ludvíková, M., Kuopio, T., & Kholová, I. (2022). PD‐L1 and PD‐1 Expression in Thyroid Follicular Epithelial Dysplasia : Hashimoto Thyroiditis Related Atypia and Potential Papillary Carcinoma Precursor. Apmis, 130(5), 276-283. https://doi.org/10.1111/apm.13218
© 2022 the Authors
Programmed cell death ligand (PD-L1)/PD-1 expression has been studied in a variety of cancers and blockage of PD-L1/PD-1 pathway is a cornerstone of immunotherapy. We studied PD-L1/PD-1 immunohistochemical expression in 47 thyroid gland specimens in groups of 1) Hashimoto thyroiditis (HT) only, 2) HT and follicular epithelial dysplasia (FED) and 3) HT, FED and papillary thyroid carcinoma (PTC). PD-1 positivity was found in immune cells, namely in lymphocytes, macrophages, and plasma cells with mean values for lymphocytes and macrophages 9% in HT group, 4% in FED group, and 4% in PTC group. PD-L1 positivity was identified in both immune cells and in the normal epithelial cells. In the HT group, mean PD-L1 staining on immune cells was 6%, in FED group 5%, and in PTC group 7%. The mean PD-L1 staining on the epithelial cells in the inflammatory parenchyma was 11.7% in HT, 13.4% in FED and 8.3% in PTC group. The mean PD-L1 staining of FED foci was 47.2% in FED group and 33.6% in PTC group. The mean tumor proportion score (TPS) was 10.4% and the mean combined positive score (CPS) was 15.5. At the moment, PTC is not a target of immunotherapy. However, understanding the complex issue of concurrent inflammation and autoimmunity can importantly influence the cancer treatment in future. ...
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Additional information about fundingThe research was funded by VTR-grant from Pirkanmaa Hospital District, Tampere Tuberculosis Foundation and Pirkanmaa Cancer Foundation (all to I.K), the Charles University Research Fund (Progres Q28/LF1 (UNCE 204013)) (to D.K.), the Charles University Research Fund (Progres Q39) (to M.L.).
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