Potential effect of IL-33/ST2 signal pathway on alveolar bone loss

• Main Authors: Aleksić Milena D. (Author), Lukić Aleksandra M. (Author)
• Format: Book
• Published: Medicinski fakultet i Klinika za stomatologiju, Niš, 2016-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 0352-5252; 1820-1202; 10.5937/asn1674611A
• Keywords: IL-33/ST2 signal pathway; alveolar bone; loss; Dentistry; RK1-715
• Source: Acta Stomatologica Naissi, Vol 32, Iss 74, Pp 1611-1622 (2016)

Introduction: ST2 is a member of IL-1R receptor family and interleukin -33 (IL-33) is its natural ligand. IL-33 functions as an 'alarmin' released upon necrotic cell death to alert the immune system to tissue damage. As ST2 receptor is expressed on many immune cells, IL-33/ST2 signal pathway has important proinflammatory or protective role in the pathogenesis of numerous diseases. IL-33/ST2 signaling promotes Th2 immune response in allergy, autoimmunity and chronic inflammatory disorders, but its role in the pathogenesis of alveolar bone loss is still unclear. We have investigated the effects of ST2 gene deletion and IL-33 administration on the periapical inflammatory bone destruction in BALB/c mice. We found that periapical lesions in ST2-/- mice are characterized by increased frequencies of CD4+ T cells, CD3+CCR6+ T cells and IFN-γ+, IL-17+, TNF-α+ and IL-6+ cells in gated CD4+ T cells compared with lesions in WT mice. A significant decrease in the percentage of CD4+ T cells producing proinflammatory cytokines and an increase in the percentage of IL-4 producing cells was observed in the periapical lesions in WT mice after IL- 33 administration. Conclusion: IL-33/ST2 signaling negatively regulates severity of periapical inflammatory bone destruction by preventing Th1/Th17 cell-mediated immune responses and indicate a possible protective role of IL-33 in the therapy of alveolar bone loss. Future research will implement new therapeuthic strategy in dental practice.