Exploring the effects of pathogen-differentiated dendritic cells in experimental periodontitis mouse model.
Periodontitis affects up to 47% of the US population. When untreated, periodontitis results in alveolar bone/tooth loss, sustaining a chronic proinflammatory disorder with cardiovascular consequences. A critical barrier to treat periodontitis relates to the regulation of protective vs. destructive immune responses. The goal of my current research is to understand the specific contribution of polymicrobial infections, Dendritic Cells (DCs) and T-cell subtypes in protective/destructive immune responses in a murine model of oral biofilm infection. Our central hypothesis is that the development of an effective adaptive immune response against oral pathogens is set in motion upon efficient recognition, processing and pathogen clearance 
by Dendritic cells. For this, DCs differentially activate, maturate and regulate a sequence of events including intracellular routing/processing, co-stimulatory molecule expression and cytokine secretion. Effective antigen presentation by mature DCs leads to polarization of CD4+ T cell response, clearance and immune homeostasis; whereas ineffective antigen presentation by immature DCs leads to sustained inflammation and bone loss characterized by strong regulatory T cells infiltration (Tregs). The expected outcome of this application is to specifically identify a protective or destructive role for DCs and T cell subsets in biofilm-induced alveolar bone loss and the mechanisms involved.
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