Dr. Michael Berton's lab studies host cell signaling pathways that regulate
inflammation and immunity, and the mechanisms that pathogens use to manipulate
and evade host immunity.
We are currently focused on the mechanisms by which the
intracellular bacterial pathogen Francisella
tularensis modulates Toll-like Receptor (TLR) signaling to evade innate immunity.
Our studies are designed to elucidate the molecular mechanisms of immune
evasion that must be considered in the development of an effective F. tularensis vaccine, and to identify
signaling mechanisms that regulate inflammatory responses at mucosal sites of
We have recently focused on novel mechanisms that negatively regulate
TLR signaling and inflammatory responses in the lung. These mechanisms may be
important in the regulation of inflammation in a variety of acute and chronic inflammatory
Morris IR, Linehan LA, Medina EA, Abplanalp AL,
Shen H, Bergman MA and Berton MT. The TLR sorting adaptor TRAM regulates TLR-dependent inflammation independently of TLR4 and TRIF. Submitted. In Revision. 2014.
Tsai SY, Segovia JA, Chang TH, Morris IR, Berton MT, Tessier PA, Tardif MR, Cesaro A, Bose S. DAMP molecule S100A9 acts as a molecular pattern to enhance inflammation during influenza A virus infection: role of DDX21-TRIF-TLR4-MyD88 pathway. PLoS Pathog. 2014 Jan;10(1):e1003848.
Rodriguez AR, Yu JJ, Guentzel MN, Navara CS, Klose KE, Forsthuber TG, Chambers JP, Berton MT, Arulanandam BP. Mast cell TLR2 signaling is crucial for effective killing of Francisella tularensis. J Immunol. 2012 Jun 1;188(11):5604-11.
EA, Morris IR, Berton MT. Phosphatidylinositol 3-kinase activation attenuates the TLR2-mediated macrophage proinflammatory cytokine response to Francisella tularensis live vaccine strain. J Immunol 2010 Dec; 185(12):7562-7572.
Abplanalp AL, Morris IR, Parida BK, Teale JM, Berton
MT. TLR-dependent control of Francisella tularensis infection and host inflammatory responses. PLoS One 2009 Nov;4(11):7920-7920.