Baltimore,
MD (5/7/99)- The discovery of a new immune mechanism believed to be at
the root of all allergies should lead to new strategies to prevent the onset
of the all too familiar sneezing, watery eyes, itchy skin and other symptoms
of allergic disease.
left: IgE
Molecule
Allergies represent an overenthusiastic reaction to outside stimuli called
allergens by the immune system. The presence of an otherwise harmless allergen
(e.g. ragweed) starts a cascade of events in the immune system involving histamine-containing
mast cells and immunoglobulin E (IgE) antibodies. Upon encountering an allergen,
the IgE triggers the mast cell to release histamine and other mediators, leading
in turn to the uncomfortable symptoms of an allergic response.
While conducting clinical trials with a new anti-IgE allergy drug called
rhuMAb-E25, researchers at Johns Hopkins University stumbled on an essential
immune system feedback loop involving IgE that appears to drive the allergic
response. While researchers had long known that IgE played a role in allergy
activation, the new research points to an equally important role played by
the hitherto unknown rise and fall of in levels of IgE receptors on basophils
and mast cells. When volunteers took an experimental drug designed to block
IgE, the amount in circulation dropped almost to zero. The researchers also
noted that the number of IgE receptors on the related immune cells also dropped
precipitously.
The patients in the study appreciated this change in terms of an absence
of allergic symptoms. But as soon as they stopped taking the drug, the symptoms
returned, along with higher levels of both IgE. Moreover, the number of IgE
receptors on basophils and mast cells increased from just a few thousand per
cell to more than 200,000 per cell. This is the first time this feedback loop
has been documented in patients.
"To stop allergies, you need to maintain low counts of both IgE antibodies
and IgE receptors. A slight increase in either restores the amount of histamine
released. This is probably true of all or most allergies," said Sarbjit
Saini, MD, leader of the Johns Hopkins research team.
Most treatments for allergy attempt to block the effects of histamine. While
these antihistamines provide relief of the symptoms of allergy, they do nothing
to interrupt the underlying causes. RhuMAb-E25 (also called Anti-IgE), the
drug evaluated in this study strikes at the root of the allergic response
by blocking IgE receptors, thereby disabling IgE. RhuMAb-E25 is a recombinant
humanized monoclonal antibody to IgE.
"Anti-IgE has the potential to prevent allergies, no matter what you're allergic
to. And it works as long as people stay on it," said Bruce Bochner, MD, also
at Johns Hopkins.
The research appears in the May 1999 issue of the Journal of Immunology.
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