Happy 50th Birthday, IgE!

A little over 50 years ago I was a research associate in the famous Biochemistry Institute in Uppsala, Sweden. I was really excited because I felt, for the first time in my career, I was at the cutting edge of molecular research doing work on ribosome methylation, and getting work published for the first time in top journals. I also knew a bunch of people there who seemed to be doing really boring work on an obscure substance called Bence Jones Protein, from the urine of a person very sick with blood cancer.

As it happened at that time, my work impressed the Nobel Prize winner, Fritz Lipman, at Rockefeller University in New York and he invited me to leave Sweden and join him to work in his department. So I continued along my merry way doing really exciting work in protein synthesis.

Meanwhile, back in Sweden, there was a huge “a-ha” moment. They found that the Bence Jones Protein was like an antibody but did not fall into any of the known classes of antibody. Brilliantly, they associated it with a substance in the blood called reagin which was known to have something to do with allergic reactions. And so IgE was born. It walks like an antibody, talks like an antibody and binds to things like an antibody. Uppsala, Sweden became the center for the identification of specific allergens that bind to IgE, and Pharmacia also located in Uppsala, developed the blood tests for allergies using these findings, the descendant of which is still in use today.

You would think in 50 years everything that could be known about the immune reaction would be known. Fast forward to the present. I received a paper about to be published, by another group in Sweden, still trying to prove a relation between IgE and allergic asthma. Their work is not in Uppsala, but in the arctic north of Sweden, a cold, dry environment where molds and dust mites have a hard time surviving. The rationale for the study is that they have been following about 3,000 kids who are now in their late teens, just like every other group of kids, except that they suffer from allergies and asthma and live in a very cold, dry climate. The predominant allergens present are cat, dog and birch.

The IgEs against other allergens, such as dust mite and mold allergens, found in milder climates, are absent. They show that the amount of each of the IgEs specific for cat and dog dander, are positively correlated with the severity of the asthma. In other words, the higher the amount of cat and dog specific IgE antibodies present, the more severe the asthma.

So far, so good. But hold on! Here’s the “bad” news. None of this bore any relationship whatsoever to whether the kid had a pet or not. A majority of the cat-sensitized kids, with current asthma, didn’t own a cat. How were they coming in contact with cat dander allergens, if they didn’t have a pet at home? They mention literature about cat allergen being persistent in the environment. Kids could come in contact with animal dander allergens at school or other places, where they frequent.

They did not have the benefit of Inspirotec’s Exhale™ to clear up the mystery. Exhale’s service performed in over 100 homes has shown that airborne dog and cat allergens, are found in my non-pet owning homes than previously thought. If when running your Exhale service, we find you have a high amount of one or both of these in your home, we will give you preventative actions to take, especially if you or your family are allergic to cat or dog allergens.

Further reading: Diagnosis of allergy by an in-vitro test for allergen antibodies. Wide L, Bennich H, Johansson SG. Lancet. 1967 Nov 25;2(7526):1105-7.Relevance of Specific IgE Antibody Titer to the Prevalence, Severity and Persistence of Asthma among 19-Year-Olds in Northern Sweden. Perzanowski MS, Ronmark E, James HR, Hedman L, Schuyler AJ, Bjerg A, Lundback B, Platts-Mills TAE. Journal of Allergy and Clinical Immunology (2016), In Press

Julian Gordon
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