The new molecule, called PAR-2, is being
studied in a research project funded by a three-year
Arthritis Research Campaign grant of more than £170,000.
“Despite the success of exciting new
treatments for RA such anti-TNF therapy, there is still
a pressing need for alternative therapies to treat the
significant population of patients who do not respond
adequately,” explained Professor John Lockhart,
Professor of Physiology at the University of the West of
Scotland.
“Understanding the biochemical
mechanisms underlying the development of autoimmunity
may provide new therapeutic avenues for RA management.”
Preliminary results suggest that the
molecule has a role in the development of RA but the
underlying mechanisms involved are unclear. The research
team, which includes Professor William Ferrell, Dr
Mohammed Nickdel and Professor Iain McInnes at the
University of Glasgow, and Professor Robin Plevin at the
University of Strathclyde, have established that PAR-2
is produced in increased quantities in RA patients with
active disease. PAR-2 acts on immune system T-cells
involved in inflammation, the cells that produce the
destructive chemicals causing tissue degeneration in the
arthritic joint. In animal models, blocking PAR-2
activation inhibited acute arthritis and halted the
production of degenerative chemicals.
Professor Lockhart hypothesises that
PAR-2 may be pivotal in the development and progression
of RA. Further research will use human tissue samples to
find out what controls PAR-2 production, how it
functions, and how it correlates with inflammation
markers.
If PAR-2 operates by changing the
body’s immune system, it may be possible to modify its
actions with the development of novel therapeutics and
provide long-term benefits for RA patients.
Rheumatoid arthritis affects around
380,000 people in the UK and is an auto-immune disease
caused by the body's immune system attacking itself. It
leads to severe joint pain, stiffness and fatigue.
Although newer, current treatments can be very
effective, they are very expensive and don't work in
everyone.