Andreas Wack

Immunoregulation Laboratory

Seasonal influenza represents a constant burden to public health, and influenza pandemics caused by new virus strains pose a serious global threat. The influenza virus causes damage to the infected lung tissue and induces an immune response which is necessary to eliminate the virus but contributes to lung pathology. A common complication of influenza is bacterial co-infection, which is associated with severe disease. Which factors tip the balance between damage or death versus successful clearance of virus and bacteria is not yet understood.

Our work aims to identify which features of the host determine the outcome of disease in influenza and in coinfection. We focus on early events after infection, and in particular on the interface between the infected epithelium and the immune system. We have established a culture system of mouse and human airway epithelium, the primary target of influenza virus, and use this system to study responses to infection with influenza virus and exposure to bacteria. Complemented by in vivo studies, this approach allows us to identify early events that pave the way for immune-mediated pathology or protection.

Mouse airway epithelial cultures

Mouse airway epithelial cultures stained with the tight junction protein ZO-1 (green) and the cilia constituent beta tubulin IV (magenta).

Selected publications

Davidson, S; McCabe, TM; Crotta, S; Gad, HH; Hessel, EM; Beinke, S; Hartmann, R and Wack, A (2016)
IFNλ is a potent anti-influenza therapeutic without the inflammatory side effects of IFNα treatment.
EMBO Molecular Medicine  8, 987-1113  PubMed abstract

Villa, M; Crotta, S; Dingwell, KS; Hirst, EMA; Gialitakis, M; Ahlfors, H; Smith, JC; Stockinger, B and Wack, A (2016)
The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis.
Nature Communications  7, 12652  PubMed abstract

Ellis, GT; Davidson, S; Crotta, S; Branzk, N; Papayannopoulos, V and Wack, A (2015)
TRAIL+ monocytes and monocyte-related cells cause lung damage and thereby increase susceptibility to influenza-Streptococcus pneumoniae coinfection .
EMBO Reports  16, 1203-1218  PubMed abstract

Wack, A; Terczyńska-Dyla, E and Hartmann, R (2015)
Guarding the frontiers: the biology of type III interferons.
Nature Immunology  16, 802-809  PubMed abstract

Davidson, S; Crotta, S; McCabe, TM and Wack, A (2014)
Pathogenic potential of interferon αβ in acute influenza infection.
Nature Communications  5, 3864  PubMed abstract

Crotta, S; Davidson, S; Mahlakoiv, T; Desmet, CJ; Buckwalter, MR; Albert, ML; Staeheli, P and Wack, A (2013)
Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.
PLOS Pathogens  9, e1003773  PubMed abstract

 

Andreas Wack

andreas.wack@crick.ac.uk
+44 (0) 20 8816 2209

  • Qualifications and history
  • 1999 PhD, MRC-NIMR and University of Konstanz, Germany
  • 1999-2009 Post doctoral fellow then group leader, Novartis Vaccines, Siena, Italy
  • 2009 Group Leader, Medical Research Council National Institute for Medical Research, London, UK
  • 2015 Group Leader, the Francis Crick Institute, London, UK