FT. LAUDERDALE, Fla. _ At the height of the hayfever season,150 sufferers in central Texas learned to say, "It's not the pollencount, stupid! It's the immunoglobulin E [IgE]."
Immunologist Tse Wen Chang, vice president of research anddevelopment at Tanox Biosystems Inc., in Houston, told the 1996Miami Bio/Technology Winter Symposium here on Monday that ahumanized chimeric antibody directed against IgE markedly relievedallergic rhinitis (hayfever) in a Phase II trial of 150 volunteersufferers.
The double-blinded, placebo-controlled, clinical study treated thepatients every two weeks for three months, including the peak pollenperiod in central Texas. The nose- and eye-dripping subjects also hadfree (though blinded) access to antihistamines, intended to "rescue"the placebo cohort from undue misery, Chang explained.
All the participants, he noted, had "high blood levels of IgE, and skinreactions to pollen."
Nasal symptoms diminished in the antibody-treated groups, as did adlibidum recourse to the "rescue" antihistamines _ but not in theplacebo cohort.
Chang subsequently told BioWorld Today that similar Phase IIstudies of the antibody, to treat allergic asthma, are getting under waywith Tanox's research partner, Ciba-Geigy Ltd., in Basel,Switzerland, in about 40 groups throughout the U.S. He added thatthe Swiss company plans to conduct Phase III trials in 1997.
"IgE causes medical disease," Chang said. "Over 26 million peoplein the U.S. alone suffer from asthma, hayfever and atopic dermatitis,severe enough to bring them to a doctor's office, and at least 5,000 ayear die of asthma." These disorders, he added, are all triggered bythe IgE immune molecule.
Chang went on to describe longer-range strategies now indevelopment at Tanox, to root out IgE at its source _ secretion by asub-group of the immune system's B lymphocytes. He pointed outthat "mice deprived of IgE live normal lives, as do human individualswith low or undetectable IgE levels." Chang discounted as"unconvincing" untested reports that IgE has a useful anti-parasiticeffect.
"Our approach for achieving the suppression of the IgE class," hesaid, "is to target IgE-expressing B cells, and mop up free IgE in theblood and lymphatics." He has identified three types of targetepitopes present on membrane-bound, IgE-specific B cells.
Once he has these antigenic bulls-eyes in his sights, Chang continued,"two approaches can be designed." One, passive immunization,employs humanized antibodies to down-regulate IgE synthesis, andremove its progenitor B cells.
Tanox is now testing in animals a more basic, active immunizationstrategy _ vaccinating patients with a recombinant peptide so theyexpress their own immune defense against the target epitopes. n
-- David N. Leff Science Editor
(c) 1997 American Health Consultants. All rights reserved.