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Multiple cells express interleukin 17 in oral squamous cell carcinoma
Author(s) -
Avadhani Avadhoot V.,
Parachuru Venkata P. B.,
Milne Trudy,
Seymour Gregory J.,
Rich Alison M.
Publication year - 2017
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12465
Subject(s) - cytokine , cytotoxic t cell , stroma , cell culture , pathology , biology , interleukin 4 , immunohistochemistry , interleukin , cell , microbiology and biotechnology , cancer research , in vitro , immunology , medicine , biochemistry , genetics
Background Interleukin ( IL )‐17 is a pro‐inflammatory cytokine with pro‐ and antitumour effects. The aim of this study was to investigate the presence and potential sources of IL ‐17 in oral squamous cell carcinoma ( OSCC ). Methods Immunohistochemistry was used to label and compare IL ‐17 + cells in the tissue sections of OSCC and inflammatory controls ( IC ), n = 14 for both. In OSCC , the comparison was made between the number of IL ‐17 + cells in the tumoral islands ( TI ), tumour–stroma interface ( TS ) and more distant stroma ( DS ). Cells expressing IL ‐17 were identified using double‐labelling immunofluorescence and examined using laser scanning microscopy. The production of IL ‐17 from tumour cells was determined in the culture supernatants of OSCC cell lines, SCC 4, SCC 15 and SCC 25, using sandwich ELISA . Results Significantly more IL ‐17 + cells were observed in OSCC compared with IC (Mann–Whitney, P < 0.0001). In OSCC , the numbers of IL ‐17 + cells were not significantly different in three compartments, TI , TS and DS (one‐way ANOVA , P > 0.05). However, the TI had significantly fewer IL ‐17 + cells than the combined stroma (both TS and DS together, Mann–Whitney, P < 0.01). Laser scanning microscopy revealed helper T cells, cytotoxic T cells, macrophages and mast cells co‐expressed IL ‐17. ELISA experiments did not detect IL ‐17 in the supernatants of OSCC cell lines. Conclusions Although the tumour cells themselves did not express IL ‐17, a range of cell types did, suggesting multiple cellular sources for IL ‐17 in OSCC . The spatial distribution of IL ‐17 + cells suggests specific interactions with cells within the tumour microenvironment, implying that IL ‐17 + cells are likely to play a role in the pathogenesis of OSCC .