ALLERGY
“FEEDBACK LOOP” IN ALLERGIC REACTIONS
Researchers testing an experimental anti-allergy drug think
that they have discovered a new immunological feedback loop
that is involved in the basic mechanism driving allergic
reactions.
The biochemical loop links the amount of IgE antibody to
the number of immune cell IgE receptors scattered on preformed
immunological mediators such as those found in mast cells.
On exposure and binding to specific allergens, IgE triggers
a cascade of biological events that leads to the allergic
reaction.
Free floating IgE is found in serum, and it is also particularly
abundant in the lungs and gastrointestinal system of people
with allergies.
In the latest research, volunteers known to have allergies
took an experimental anti-IgE drug. Over time, the amount
of circulating IgE in their blood decreased by as much as
99%. Previously it had been thought that anti-IgE drugs
worked by blocking the binding of IgE to receptors which,
in turn, blocked the receptor-mediated allergic response.
But researchers found that the number of IgE receptors on
certain immune cells decreased in tandem with the drop in
free floating IgE antibodies, indicating that the quantity
of the antibodies and the IgE receptors closely correspond
to each other.
“To stop allergies, you need to maintain low counts
of both IgE antibodies and IgE receptors,” said Dr
Sarbjit Saini, the study’s lead author. “A slight
increase in either restores the amount of histamine released.”
Anti-IgE antibodies, which have been in clinical development
for several years, work by binding to the same region of
the IgE receptor that is typically used by the IgE molecule.
The anti-IgE antibodies end up “complexing”
with free floating IgE in a person’s serum and in
so doing, eliminate the ability of IgE molecules to bind
to cells containing inflammatory mediators.
BMJ no 7194 15th May 1999
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