Director, Lydia Becker Institute of Immunology and Inflammation

Professor of Inflammatory Disease

2nd floor, Core Technology Facility

University of Manchester

Oxford Road

Manchester

M13 9PT

1. MRC NC3Rs panel member for project grants and studentships.
2. Chair – Research Council of Norway
3. Trustee and education secretary of the British society For Immunology since February 2007.
4. Scientific Advisory Board Member for Topigen plc Canada.
5. Strategy Committee, Kennedy Institute 2004-2008.
6. Strategy Committee for the Centre for Respiratory Infection since 2009.
7. Arthritis Research Campaign Research sub-committee April 2005 -2008.
8. Editor of Viral Immunology since October 1999.
9. Editor of Microbes and Infection since 2001.
10. Editor of Immunology since 1999.
11. Associate Editor of Mucosal Immunology since January 2007.
12. External examiner for King’s MSC in Immunology and Infection since July 2009.
13 Central Biological Services Chair since 2008.
14. Member of Asthma UK’s research committee September 2007 – August 2011.
15. Member of the British Society of Immunology since 1989.
16. Member of the Society for Mucosal Immunology since 1996.
17. Committee member of the Antibody Club since 1995
18. Meetings committee member of the British Society for Immunology since December 1999.
19. American association of immunologists since April 2001
20. Member of the Medical Research Club since 2005.
21. Member of the Expert Review Group 4 Wellcome Trust

The group has internationally competitive research in the following areas:

1. How immunological homeostasis is maintained in the respiratory tract.  This basic immunology programme feeds into all aspects inflammatory disease.  We have published evidence that the default state of lung innate immunity is activation and that it is restrained by the local microenvironment, predominantly by factors expressed or secreted by the respiratory epithelium. This overall hypothesis leads into the following areas of investigation:

a) Factors expressed or secreted by the respiratory epithelium that regulate innate immunity.

b) The impact of genetic deletion of factors expressed or secreted by the respiratoryepithelium on innate immune activity in the steady state and during acute inflammation.

c) Analysis of the unique phenotype of alveolar macrophages.

2. The consequences of altered homeostasis following resolution of acute inflammation or during allergy.  We have established models for the following infections:Influenza virus (H1N1, H3N2 and H5N1), Respiratory Syncytial virus, Streptococcus pneumoniae, Haemophilus influenzae and Pseudomonas aeruginosa, Cryptococcus neoformans and Aspergillus. All provide acute infection of varying severity depending on the dose of pathogen, the age of the host and the strain of mouse used. Further we are part of the MOSAIC consortium analysing the pathogenesis of recent avian influenza viruses in humans. The projects leading on from resolution of these acute infections include:

a) Analysis of long term alterations in innate immune subsets, particularly airway macrophages

b) Alteration of the commensal microbial flora by these acute infection (by 16s ribosomal RNA sequencing)

c) Altered epithelial and endothelial control and permeability

d) Changes in micro inhibitory RNA species in respiratory epithelial cells and macrophages

e) Parameters contributing to susceptibility to secondary bacterial pneumonia

f) control of pathogens in the allergic lung

3. Novel pathways of innate immune regulation in the steady state and post acute inflammation.  These novel pathways (envisaged to lead to translatable compounds and processes) include: a) TAM receptors, b) Interleukin 33 and its receptor, ST2L, c) IL-10 receptor, d) transforming growth factor beta receptor, e) micro-inhibitory RNA species, f) CD200 and its receptor and g) TREM1 and 2

4.. Therapeutic modulation of acute and chronic inflammation.We have developed pre-clinical data showing the relative advantages of a number of compounds compared to those currently in use.  For example, in collaboration with GSK we have defined a reduced infectious risk using agents that only block TNFR1 compared to etanercept (widely used in the treatment of arthritis) that blocks TNFR1 and TNFR2.  Reduced infectious risk provides new and developing reagents with a market advantage.

We have also identified OX40 blockade as a realistic replacement for anti-TNF therapy in acute infectious, and chronic autoimmune, disease.  The treatment only targets recently activated antigen specific T cells and so once again reduces the infectious risk in treated patients. This work is in collaboration with UCB Celltech.  The list continues with reagents that harness innate negative regulators such as CD200 receptor (in collaboration with Neil Barclay, Oxford), inhibition of reactive oxygen and nitrogen species (in collaboration with Storm bio, New Jersey) and we are currently trialling micro-inhibitory RNA species in smoke-induced exacerbation of human COPD (In collaboration with Trevor Hansel, Imperial College).

Professor Tracy Hussell Tracy Hussell completed her PhD at University College London where she identified Helicobacter pylori as an aetiological agent in human gut lymphomas. After her PhD Professor Hussell moved to Respiratory Medicine at St Mary's Hospital to study immunity and pathology to respiratory syncytial virus. In 1998 she accepted a lectureship in the Centre for Molecular Microbiology and Infection (CMMI) at Imperial College led by Professors Gordon Dougan and Douglas Young. She was subsequently awarded a career development fellowship by the Medical Research Council. Professor Hussell was awarded a Personal Chair in inflammatory disease at Imperial College London in 2006 and has developed a vibrant research group studying immune health and its deregulation in the lung. Professor Hussell is currently the Director of the Lydia Becker Institute of Immunology and Inflammation at the University of Manchester.

• 2002: Certificate of advanced studies in learning and teaching. Imperial College London,
• 1990 -1994: PhD (July 1994): Immunology., Faculty of Clinical Sciences, UCL Medical School
• 1985 – 1989: B.Sc.(Hons.), Applied Biology, (2:1)., Nottingham University.
• 1983 – 1985: OND in Science., Worcester Technical College, Worcester. Mathematics (distinction), Physics (merit), Biology (distinction), Chemistry (merit), Microbiology (merit).