| A predominant clinical feature of allergic
disease is a persistent inflammation at the site of disease. In asthma,
inflammation is localized to the airway wall. Currently, it is thought that
inflammatory cells (white blood cells) induce asthma by releasing substances
that damage the lining of the airways and induce constriction (narrowing
of the airways), mucus production and remodeling of tissue. The inflammatory
response in the asthmatic lung and in other allergic diseases is a very
complex mixture of cells and molecules and it is not clear which factors
play the major role in inducing disease.
Allergic asthma is recognized as a chronic inflammatory disease of the
airways that is characterized by reversible airways obstruction in association
with aberrant CD4+T helper 2 (Th2 cell) lymphocyte responses to common
environmental stimuli. Indeed, the hallmark features of allergic asthma,
elevated serum immunoglobulin E (IgE), mucus hypersecretion, eosinophilia
and enhanced bronchial reactivity (airways hyperreactivity [AHR]) to non-specific
spasmogenic stimuli have all been linked to the effector functions of
Th2 cytokines (e.g. interleukin- (IL)-4, 5, 9, 10 and 13). Collectively,
it is these pathogenic processes that are thought to promote airways obstruction
in asthma, which predisposes to wheezing, shortness of breath and life-threatening
limitations in airflow. Th2 mediated immune processes have also linked
to the pathogenesis of allergic diseases of the gastrointestinal tract.
Viral infections of the lung play a key role in exacerbating asthma and
eosinophils and T -lymphocytes are also thought to underpin aspects of
viral induced asthmatic episodes.
Research in our Group focuses on two major areas:
1. Identifying the key cells and molecules, which underpin the pathogenesis
of allergic disease of the lung, skin and gastrointestinal tracts and
those that underpin the pathogenesis of respiratory viral infections.
2. Developing strategies that will direct the immune response away from
the harmful Th2 inflammatory response to that which is protective or non-responsive.
The long-term goal of this research is to identify novel therapeutic approaches
for the treatment of asthma and allergy and viral-induced disease of the
lung.
Our experimental approach integrative, employing state-of-the-art molecular
genetic techniques in association with model systems to identify the role
of inflammatory cells and molecules in the events that underpin disease.
Projects within the group focus on the role of individual Th2 cytokines
in disease pathogenesis and characterization of the downstream signaling
pathways employed by theses molecules to induce disease.
We continue to act as a national reference centre for the diagnosis of
MH susceptibility.
Contact Information
PO Box 334 (Mills Road) Building 54
Canberra City, ACT 2601
AUSTRALIA
Telephone: (61-2) 6125 2032 Facsimile: (61-2) 6125 0415
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