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Forkhead box P3‐positive regulatory T‐cells and interleukin 17‐positive T‐helper 17 cells in chronic inflammatory periodontal disease
Author(s) -
Parachuru V. P. B.,
Coates D. E.,
Milne T. J.,
Hussaini H. M.,
Rich A. M.,
Seymour G. J.
Publication year - 2014
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12169
Subject(s) - foxp3 , inflammation , immune system , immunology , t cell , interleukin , cd19 , interleukin 17 , medicine , biology , chemistry , cytokine
Background and Objective The role of two recently identified and closely related T‐helper cell subsets – regulatory T‐cells [Tregs; forkhead box P3‐positive ( FOXP 3 + )] and Th17 cells [interleukin‐17‐positive ( IL‐ 17 + )] – in periodontal disease is yet to be determined. Tregs are essential in maintaining peripheral tolerance and regulating the immune response. Th17 cells play a critical role in several autoimmune diseases, inflammation and host defence. The aim of this study was to determine the presence of FOXP 3 + Tregs and IL‐ 17 + cells, and their possible spatial interaction, in diseased periodontal tissues. Material and Methods Twenty‐nine archival tissues with nonspecific gingival inflammation were grouped based on the intensity (minimally or intensely inflamed) and nature (T‐cell predominant or B‐ and plasma‐cell predominant) of the inflammatory infiltrate. Using double‐labelling immunohistochemistry, the concomitant presence of FOXP 3 + and IL‐ 17 + cells was determined and their spatial relationship was established. In addition, the proportions of FOXP 3 + and IL‐ 17 + cells were compared between the groups. Results Of the 29 gingival specimens investigated, 17 were intensely inflamed (≥ 1000 inflammatory cells per 0.12 mm 2 ) and 12 were minimally inflamed (≤ 600 cells per 0.12 mm 2 ). Based on the percentage of CD 19 + B‐cells and plasma cells collectively and CD 3 + T‐cells, gingival tissues were also grouped into B‐ and plasma‐cell‐predominant gingival tissues ( n = 21; 50.7% total B‐ and plasma cells vs. 19.1% T cells; p < 0.001) and T‐cell‐predominant gingival tissues ( n = 8; 61.0% T‐cells vs. 15.2% B‐ and plasma cells; p = 0.007). More FOXP 3 + cells than IL‐ 17 + cells were observed in all archival gingival tissues examined. A trend towards an increased number of FOXP 3 + cells was observed for intensely inflamed gingival tissues (6.7%) and for B‐ and plasma‐cell‐predominant tissues (6.4%) compared with minimally inflamed gingival tissues (4.6%) and T‐cell‐predominant gingival tissues (4.5%). However, no statistically significant difference in the mean percentage of FOXP 3 + cells between the groups was observed. Interestingly, FOXP 3 + cells were significantly correlated with the B‐ and plasma‐cell/T‐cell ratio in B‐ and plasma‐cell‐predominant tissues ( r = 0.713, p < 0.001). Overall, there were very few IL‐ 17 + cells (< 1%). All IL‐ 17 + cells identified in this study had an ovoid/plasmacytoid morphology and were larger in size compared with adjacent inflammatory cells. IL‐ 17 + and FOXP 3 + cells were not adjacent to each other in any of the areas examined, suggesting that FOXP 3 + Tregs do not directly interact with IL‐ 17 + cells in diseased gingival tissues. IL‐ 17 + / FOXP 3 + cells were not detected in the tissues examined. Conclusion These results show that FOXP 3 + cells are more prominent than IL‐ 17 + cells in periodontal disease processes, which may suggest a predominant role for FOXP 3 + cells in periodontal disease. Further studies are required to characterize these cells more precisely and to understand, in more detail, their roles in the pathophysiology of periodontal disease.