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Edmond scientist discovers hidden antibodies in mice

A discovery by an Oklahoma Medical Research scientist has discredited the 50-year-old accepted dogma that disease fighting cells in the body carry only one protein.

Edmond’s Patrick Wilson has discovered that B cells can make a mistake when the cells bind to human tissue and change receptors. Cells changing receptors sometimes may result in a second allele (chromosome) producing a second antibody protein, he found. Wilson revealed that 10 percent of mouse models use both alleles.

Wilson’s research paper appears in a recent issue of The Journal of Experimental Medicine. An editorial in that publication by Rockefeller University researcher Ruth Williams described Wilson’s discovery as tantamount to exposing “a wolf in sheep’s clothing.”

Wilson’s wife, Nai-Ying Zheng, manages the lab at OMRF and was part of Wilson’s research team. Dr. Rafael Casellas of the National Institutes of Health in Bethesda, Md., was Wilson’s major collaborator in the project. Other participants were Qingzhao Zhang, Melissa D. Mathias and Kenneth Smith.

“It changes the paradigm of immunology. It changes our idea of it,” said Wilson, who earned his doctorate from the University of Texas Southwestern Medical Center in Dallas and did his postdoctoral studies at the Rockefeller University in New York City.

“It’s not true one B cell is always expressing a single receptor. Many B cells can express two. These potentially are the ones that cause autoimmune disease later.”

B cells are white blood cells that defend the human body by creating antibody proteins to protect people with immune protection from disease and infection. Antibodies bind to bacteria, viruses and pathogens, thus blocking their ability to attach to tissue.

“The other thing it does — it tells our body (B cells) are there and other cells will then destroy the pathogens,” Wilson explained.

For the system to work properly, every healthy B cell produces only one antibody protein so it can be deleted if it binds to human tissue.

Despite these mechanisms, 28 million people a year are diagnosed with an autoimmune disease, Wilson said. Autoimmune diseases include a variety of diseases such as lupus, rheumatoid arthritis, multiple sclerosis and Graves disease — among others.

His research shines new light on how cells survive in spite of being autoreactive.

“One thing that’s important to figure out is how are these B cells are escaping these mechanisms. How are they avoiding either changing their receptor or just being auto reactive and still surviving — not being removed from the repertoire so they can be dangerous,” Wilson said.

The next step of his investigation will try proving if these are indeed the cells causing autoimmune disease in the mice models. A third step will involve looking for the same disease processes in humans.

It remains too early to envision creating specific pharmacological drugs based on the research to fight autoimmune diseases, he said. But his basic scientific research may be the first step in finding new, successful treatments.

Source: The Edmond Sun - Associated Press content © 2007. All rights reserved.

Hi Bromley,

I've read this post several times, but I'm not sure I fully understand the science behind it.
If I try and explain to you what I think it means, I'd be really grateful if you could point out where I've got it wrong:

An antibody normally has one type of protein, (or peptide chain), on its surface, so that it binds to one specific antigen.

If the protein on an antibody's surface matches the body's own tissue, it will be destroyed.

Some B-cells have two types of protein on the surface -- one for self tissue, the other for "foreign" tissue.

Because they are not exclusively aimed at self tissue, they are not destroyed.

They can attach to self tissue and trigger an attack, or even act as the glue between foreign and self tissue.

That's my interpretation of this finding but I'm really not confident about my understanding... any help would be greatly appreciated!

Dom. [/i]