Immunity during inflammation
Research in this area:
This group of researchers is based in the Kennedy Institute of Rheumatology and investigates immune dyregulation during inflammation.
Excessive immune responses, such as those experienced during infection or autoimmunity, contribute significantly to death and disability world wide.
Our research aims to alleviate inflammation by:
- Targeting novel inflammatory markers (OX40).
- Harnessing endogenous inhibitory molecules (CD200, TGF, Sirps).
- Educating the affected environment by innate imprinting.
The inflammatory conditions used include in vivo pulmonary models of influenza and respiratory syncytial viruses, Cryptococcus neoformans, Chlamydia pneumoniae and BCG.
We also investigate the effect of therapeutic manipulations on the initiation or relapse of rhematid arthritis.
Recently, we have demonstrated that OX40 represents a potent therapeutic target during respiratory infectious disease, preventing clinical symptoms without hindering pathogen clearance.
We have also developed the novel concept of innate imprinting whereby organs devoid of lymphoid tissue (such as the airways and joints) are 'trained' to regulate incoming lymphocytic infiltrates. Such imprinting is long lasting and provides generic protection against a variety of infectious and autoimmune inflammatory disorders.
Dr Tracy Hussell
Selected publications:
- Stimulation via Toll-like receptor 9 reduces Cryptococcus neoformans-induced pulmonary inflammation in an IL-12-dependent manner. Edwards L, Williams AE, Krieg Am, Rae AJ, Snelgrove RJ & Hussell T. Eur J Immunol 2005; 35:273-281.
- Innate imprinting by the modified heat-labile toxin of Escherichia coli (LTK63) provides generic protection against lung infectious disease. Williams AE, Edwards L, Humphreys IR, Snelgrove R, Rae A, Rappuoli R & Hussell T. J Immunol 2004; 173:7435-7443.
- A critical role for OX40 in T cell-mediated immunopathology during lung viral infection. Humphreys IR, Walzl G, Edwards L, Rae AJ, Hill S & Hussell T. J Exp Med 2003; 198:1-7.
- OX40 ligation on activated T cells enhances the control of Cryptococcus neoformans and reduces pulmonary eosinophilia. Humphreys IR, Edwards L, Walz GI, Rae Aj, Dougan G, Hill S & Hussell T. J Immunol 2003; 170:6125-6132.
