Innate Immunity and tissue injury

Our research encompasses the molecular mechanisms underlying the development of tissue injury by immune-mediated mechanisms and the characterization of the main chemical mediators recruited upon engagement of receptors for both pathogen-associated molecular patterns and receptors for the Fc portion of IgG class antibodies. The cooperation between these receptors helps explain the current models of function of the immune system, where poorly soluble ligands and particulate stimuli are the driving force of the acute inflammatory reaction and the initiation of the adaptive immune response. These facts are clinically relevant for the pathogenesis of autoimmune, and autoinflammatory diseases and the defense against microbial infection. Our most recent research focuses on the mechanisms of transcripcional regulation of the cytokines Il-10, Il-12 p70 and IL-23.