Complement receptor 3-dependent engagement by β-glucan modulates dendritic cells to induce regulatory T-cell expansion.

is an important pathogen causing invasive infection associated with a high mortality rate. One mechanism that causes the failure of eradication is an increase in regulatory T cells (Treg), which play a major role in immune suppression and promoting pathogenicity. To date, how induces a Treg response remains unclear.

In-depth investigation of FAM20A insufficiency effects on deciduous dental pulp cells: Altered behaviours, osteogenic differentiation, and inflammatory gene expression.

Aim: Loss-of-function mutations in FAM20A result in amelogenesis imperfecta IG (AI1G) or enamel-renal syndrome, characterized by hypoplastic enamel, ectopic calcification, and gingival hyperplasia, with some cases reporting spontaneous tooth infection. Despite previous reports on the consequence of FAM20A reduction in gingival fibroblasts and transcriptome analyses of AI1G pulp tissues, suggesting its involvement in mineralization and infection, its role in deciduous dental pulp cells (DDP) remains unreported. The aim of this study was to evaluate the properties of DDP obtained from an AI1G patient, providing additional insights into the effects of FAM20A on the mineralization of DDP.

Deep dental phenotyping and a novel FAM20A variant in patients with amelogenesis imperfecta type IG.

Objectives: To identify etiologic variants and perform deep dental phenotyping in patients with amelogenesis imperfecta (AI).

Methods: Three patients of two unrelated families were evaluated. Genetic variants were investigated by exome and Sanger sequencing.