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NEWPORT - An Oregon State University expert on allergies - who also is an allergy sufferer - recently explained his latest research findings on allergies to more than 120 nurses at the annual meeting of the Northwest Society of Allergy Nurses.

Continued progress in basic research, he says, may one day soon lead to approaches that can interrupt the complex biochemical cycle which leads to an unwanted allergic response.

Anthony Vella, an assistant professor of microbiology and affiliate with the Linus Pauling Institute at OSU, said at the meeting that he understands the need for better therapies. After spending his second spring here, Vella said he became sensitized to the allergens in Oregon and succumbed to the usual coughing, congestion and tearing.

Vella joined the Linus Pauling Institute from The National Jewish Center for Immunology in Denver, Colo., just two years ago and brings a wealth of expertise on the role of the immune system in allergic reactions.

According to Vella, most allergic reactions can be traced to a specific type of "T cell," which responds to a host of environmental particles like dust, mold and pollen. T cells are essential components of the immune system that enable us to fight infection and cancer. However, increasing evidence shows that some T cells are also implicated in allergic responses and autoimmune diseases like multiple sclerosis and arthritis.

"Research has shown that a T cell called Th2 is largely responsible for sustaining allergic reactions over time," said Vella. "The Th2 cell makes a molecule called interleukin-4 that drives the allergic episode."

He explained that Th2 cells help activate another type of immune cells - "B cells" - which are front-line troops of the immune system that bind bacterial toxins as well as allergins. B cells produce antibodies, also called immunoglobulins, that fight pathogens. B cells often produce an antibody called IgE in response to irritating allergins. IgE in turn causes mast cells in the blood to degranulate and release histamine molecules as part of an inflammatory cascade that culminates in allergic symptoms.

Those symptoms, Vella said, vary depending on where the mast cells degranulate. For example, when mast cells in the intestine bind IgE in response to food allergins, the inflammatory process may result in diarrhea. On the other hand, mast cells in the skin can cause hives when they degranulate. In the sinuses and lungs, mast cell degranulation may cause hay fever symptoms. The process is complex.

"Th2 cells activate B cells by producing a molecule called interleukin-4," explained Vella. "Il-4 binds to the B cell and causes it to produce IgE. Il-4 also helps Th2 cells stay alive. So the Th2 cell recapitulates its own existence by producing Il-4."

Vella and his co-workers discovered that interleukin-4 blocks T cell death by dismantling a specific"death" pathway that T cells activate in order to die. He believes that interleukin-4 may be a self-sustaining "survival factor" that allergy-inducing T cells utilize to perpetuate their own existence, enabling them to drive allergic reactions.

Vella said he envisions a drug or nutritional therapy in the near future that could block the ongoing survival of the Th2 cells, which is induced by interleukin-4. Such a drug could be used temporarily during the peak of the allergy season, and would ideally preclude the whole inflammatory cascade before it begins, without the side effects associated with antihistamines. Antihistamines, Vella said, exert their effect much further downstream. They neutralize histamine molecules released by mast cells in the blood as part of the inflammatory cascade driven by the T cells and Il-4. "It would be much more effective to arrest the allergic response at the onset rather than try to subdue it with poorly understood antihistamine drugs that have not proven very effective," he said.