CGB - Universidad Mayor

11 marzo 2020

Interleukin-35 inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis.

DOI : 10.1111/jcpe.13282


AIM: T lymphocytes play a central role during the pathogenesis of periodontitis,

and the imbalance between the pathogenic T-helper type 17 (Th17) and protective

T-regulatory (Treg) lymphocytes determines the tooth-supporting alveolar bone

resorption. Interleukin (IL)-35 is a novel anti-inflammatory cytokine with

therapeutic properties in diseases whose pathogenesis is associated with the

Th17/Treg imbalance; however, its role during periodontitis has not been

established yet. This study aimed to elucidate whether IL-35 inhibits the

alveolar bone resorption during periodontitis by modulating the Th17/Treg


MATERIALS AND METHODS: Mice with ligature-induced periodontitis were treated

with locally or systemically administrated IL-35. As controls,

periodontitis-affected mice without IL-35 treatment and non-ligated mice were

used. Alveolar bone resorption was measured by micro-computed tomography and

scanning electron microscopy. The Th17/Treg pattern of the immune response was

analysed by qPCR, ELISA, and flow cytometry.

RESULTS: IL-35 inhibited alveolar bone resorption in periodontitis mice.

Besides, IL-35 induced less detection of Th17 lymphocytes and production of

Th17-related cytokines, together with higher detection of Treg lymphocytes and

production of Treg-related cytokines in periodontitis-affected tissues.

CONCLUSION: IL-35 is beneficial in the regulation of periodontitis;

particularly, IL-35 inhibited alveolar bone resorption and this inhibition was

closely associated with modulation of the periodontal Th17/Treg imbalance.

Investigadores Participantes del Centro



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