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Basic biology and role of interleukin‐17 in immunity and inflammation
Author(s) -
Zenobia Camille,
Hajishengallis George
Publication year - 2015
Publication title -
periodontology 2000
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.725
H-Index - 122
eISSN - 1600-0757
pISSN - 0906-6713
DOI - 10.1111/prd.12083
Subject(s) - medicine , rheumatoid arthritis , immunology , periodontitis , inflammation , interleukin 17 , cytokine , psoriasis , interleukin , pathogenesis , arthritis , disease , interleukin 23 , pathology
Interleukin‐17 (also known as interleukin‐17A) is a key cytokine that links T‐cell activation to neutrophil mobilization and activation. As such, interleukin‐17 can mediate protective innate immunity to pathogens or contribute to the pathogenesis of inflammatory diseases, such as psoriasis and rheumatoid arthritis. This review summarizes the basic biology of interleukin‐17 and discusses its emerging role in periodontal disease. The current burden of evidence from human and animal model studies suggests that the net effect of interleukin‐17 signaling promotes disease development. In addition to promoting neutrophilic inflammation, interleukin‐17 has potent pro‐osteoclastogenic effects that are likely to contribute to the pathogenesis of periodontitis, rheumatoid arthritis and other diseases involving bone immunopathology. Systemic treatments with anti‐interleukin‐17 biologics have shown promising results in clinical trials for psoriasis and rheumatoid arthritis; however, their impact on the highly prevalent periodontal disease has not been investigated or reported. Future clinical trials, preferably using locally administered interleukin‐17 blockers, are required to implicate conclusivelyinterleukin‐17 in periodontitis and, more importantly, to establish an effective adjunctive treatment for this oral inflammatory disease.