Frederic Geissmann

TL;DR: Experimental evidence indicates that monocytes are innate effectors of the inflammatory response to microbes, killing pathogens via phagocytosis, the production of reactive oxygen species (ROS), nitric oxide (NO), myeloperoxidase and inflammatory cytokines and can both stimulate and suppress T-cell responses in infectious and autoimmune diseases.

TL;DR: It is shown that dissemination and poor prognosis are associated with lack of E‐cadherin expression on LCH cells, and Aggressive clinical evolution of LCH may be related to the loss of functions mediated by E‐ caderin.

TL;DR: It is found that inflammatory ly6C+ monocytes and neutrophils largely mediated memory CD8+ T cell bacteriocidal activity by producing increased levels of reactive oxygen species (ROS), augmenting the pH of their phagosomes and inducing antimicrobial autophagy.

TL;DR: Using the ciliopathic Fuz mutant mouse, the etiology for a common craniofacial anomaly is elucidated and links between two classes of human disease: FGF-hyperactivation syndromes and ciliopathies are identified.

TL;DR: The findings do not support the hypothesis of a role of EBV, CMV, or HHV-6 in the pathogenesis of LCH, and indicate that the frequent detection of Epstein-barr virus (EBV) in Langerhans cell histiocytosis is accounted for by the infection of bystander B lymphocytes in LCH granuloma.