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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.
Key words:
IL-33/ST2 signal pathway, alveolar
bone, loss
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