IL-23-producing CD68+ macrophage-like cells predominate within an IL-17-polarized infiltrate in chronic periodontitis lesions

• Published in: Journal of clinical periodontology Vol. 38; no. 10; pp. 879 - 886
• Main Authors: Allam, Jean-Pierre, Duan, Yonggang, Heinemann, Friedhelm, Winter, Jochen, Götz, Werner, Deschner, James, Wenghoefer, Matthias, Bieber, Thomas, Jepsen, Soren, Novak, Natalija
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.10.2011; Blackwell
• Subjects: Aged; Antigen-Presenting Cells - cytology; Antigen-Presenting Cells - immunology; Antigen-Presenting Cells - metabolism; Antigens, CD - immunology; Antigens, CD20 - immunology; Antigens, Differentiation, Myelomonocytic - immunology; B-Lymphocytes - immunology; Biological and medical sciences; Chronic periodontitis; Chronic Periodontitis - immunology; Chronic Periodontitis - pathology; Dentistry; Facial bones, jaws, teeth, parodontium: diseases, semeiology; Female; Flow Cytometry; Fluorescent Antibody Technique; Humans; IL-17; IL-23; Interleukin-17 - immunology; Interleukin-23 - biosynthesis; Interleukin-23 Subunit p19 - immunology; Langerhans cells; Lipopolysaccharides; macrophages; Macrophages - immunology; Macrophages - metabolism; Male; Medical sciences; Middle Aged; Mouth Mucosa - immunology; Mouth Mucosa - pathology; Non tumoral diseases; oral mucosa; Otorhinolaryngology. Stomatology; Porphyromonas gingivalis - immunology; Real-Time Polymerase Chain Reaction; Th17 Cells - immunology; Toll-Like Receptor 4 - physiology; Chronic periodontitis; Stomatology; oral mucosa; Mucosa; Dentistry; IL-23; Oral cavity; Periodontal disease; Chronic; macrophages; Langerhans cell; Periodontitis; IL-17; Langerhans cells; Lesion; Macrophage
• ISSN: 0303-6979; 1600-051X
• DOI: 10.1111/j.1600-051X.2011.01752.x

Allam JP, Duan Y, Heinemann F, Winter J, Götz W, Deschner J, Wenghoefer M, Bieber T, Jepsen S, Novak N. IL‐23 producing CD68+ macrophage‐like cells predominate within a IL‐17 polarized infiltrate in chronic periodontitis lesions. J Clin Periodontol 2011; 38: 879–886. 38: 879–886. doi: 10.1111/j.1600‐051X.2011.01752.x. Aim: To analyse antigen‐presenting cells (APCs), such as dendritic cells (DCs), macrophages (Mo) or B cells depending on the regional site of chronic periodontitis (CP), and to investigate their relation to Th17 cells. Material and Methods: Biopsies from oral mucosa as well as the coronal and bottom regions of CP were analysed by immunhistochemistry, immunofluorescence, flow cytometry and real‐time PCR. Results: A predominance of CD68+ Mo‐like cells and CD20+ B cells and strong Th17 infiltration was observed in the bottom region of CP lesions, while CD1a+ DCs were only detected in the coronal regions, where Th17 infiltration was low. Furthermore, CD68+ Mo‐like cells displayed CD163 expression as a typical Mo‐marker, but expressed in parallel typical DCs markers, such as CD11c or CD209 and TLR4. Interestingly, Th17‐inducing cytokine IL‐23p19 was produced by CD68+ Mo‐like cells, but not CD20+ B cells. Moreover, the stimulation of in vitro generated CD68+ Mo‐like cells by Porphyromonas gingivalis‐derived (Pg) lipopolysaccharide resulted in the upregulation of their IL‐23p19 mRNA expression, which was inhibited by the blockage of TLR4. Conclusions: In view of these data, a picture emerges that IL‐17‐producing cells in CP could be in part directed by CD68+ Mo‐like cells, which produce IL‐23p19 upon TLR4 activation by Pg.