Joseph Mizgerd

Pulmonary Center, Boston University School of Medicine, United States of America

Joseph Mizgerd is Professor of Medicine and Microbiology at Boston University School of Medicine.

He is mainly interested in the processes of neutrophil emigration and activation in the lungs. Major focuses of his current work are the roles played by NF-kappaB and STAT3 transcription factors in dictating the expression of innate immunity genes in the lungs, in directing neutrophil emigration and activation, and in balancing the protective and destructive effects of pulmonary inflammatory responses.

Any competing interests declared are displayed with individual evaluations.

Faculty Member: Respiratory Disorders > Respiratory Infections (since 29 November 2006)

Links

http://www.hsph.harvard.edu/mizgerdlab/

All recent recommendations

• 3.0
  Toll-like receptor 1 polymorphisms affect innate immune responses and outcomes in sepsis.
  Recommended by Joseph Mizgerd
  
• 4.8
  Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness.
  Recommended by Joseph Mizgerd, Ralph Corey
  
• 6.0
  Citrullination of CXCL8 by peptidylarginine deiminase alters receptor usage, prevents proteolysis, and dampens tissue inflammation.
  Recommended by Joseph Mizgerd
  
• 3.0
  Interleukin 1{alpha}-induced NF{kappa}B Activation and Chemokine mRNA Stabilization Diverge at IRAK1.
  Recommended by Joseph Mizgerd
  
• 6.7
  Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome.
  Recommended by Joseph Mizgerd, Lars Rogge, Jonathan Dyer, Michelle Lowes with Kristine E Nograles
  
• 6.0
  IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia.
  Recommended by Joseph Mizgerd
  
• 3.0
  Mouse models of rhinovirus-induced disease and exacerbation of allergic airway inflammation.
  Recommended by Joseph Mizgerd
  
• 3.0
  Expression of the 1918 influenza A virus PB1-F2 enhances the pathogenesis of viral and secondary bacterial pneumonia.
  Recommended by Joseph Mizgerd
  
• 3.0
  Selective predisposition to bacterial infections in IRAK-4-deficient children: IRAK-4-dependent TLRs are otherwise redundant in protective immunity.
  Recommended by Joseph Mizgerd
  
• 6.0
  Differential role of TLR- and RLR-signaling in the immune responses to influenza A virus infection and vaccination.
  Recommended by Joseph Mizgerd
  
• 3.0
  Interleukin-6 dependent survival of multiple myeloma cells involves the Stat3-mediated induction of microRNA-21 through a highly conserved enhancer.
  Recommended by Joseph Mizgerd
  
• 4.8
  Staphylococcus aureus Panton-Valentine leukocidin causes necrotizing pneumonia.
  Recommended by Joseph Mizgerd, Thomas Dougherty
  
• 3.0
  The humoral pattern recognition receptor PTX3 is stored in neutrophil granules and localizes in extracellular traps.
  Recommended by Joseph Mizgerd
  
• 3.0
  Role of host cytokine responses in the pathogenesis of avian H5N1 influenza viruses in mice.
  Recommended by Joseph Mizgerd
  
• 3.0
  A novel host defense system of airways is defective in cystic fibrosis.
  Recommended by Joseph Mizgerd
  
• 3.0
  Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides.
  Recommended by Joseph Mizgerd
  
• 3.2
  Sepsis-induced suppression of lung innate immunity is mediated by IRAK-M.
  Recommended by Joseph Mizgerd, Helena Tlaskalova-Hogenova