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Medical Research news

Bee sting venom can help develop immunity to bee stings

Bee stings can be painful, and for people who are allergic to the bee's venom, they can be deadly. But a new study from Yale School of Medicine finds that the key toxic component in bee venom - the major allergen - can actually induce immunity and protect against future allergic reactions to the toxin. The study appears in the Cell Press journal, Immunity.
The Yale research team examined the effect in mice of an allergic component called Phospholipase A2 (PLA2). They found that, once detected by the innate immune system of the mice, the PLA2 triggered a cascade of immune responses designed to fight the intruding toxin.

The researchers then examined whether repeated exposure to PLA2 could induce a longstanding antibody response, and confer immunity. They repeatedly immunized the mice with doses of PLA2 and found that the mice were protected from the damaging effects of an allergic reaction.

"These findings support the argument that allergic responses evolved to protect us from noxious environmental substances," said senior author Ruslan Medzhitov, professor of immunobiology at Yale School of Medicine and a Howard Hughes Medical Institute investigator.

Venoms are very common in nature. "They are used for defense and for predation," Medzhitov explains. Therefore, he says, the Yale study may put the unpleasant sensation most people experience with bee stings into a new light. "It should not be very surprising that animals developed defenses against venoms, and our study indicates that allergic immunity is one of these defenses."

Medzhitov cautions, however, that when the allergic response over-reacts, it can lead to a dangerous condition known as anaphylactic shock. "We found that there is a very thin line between protective and potentially life-threatening allergic reactions to bee venom."

Other authors are Noah W. Palm, Rachel Rosenstein, Shuang Yu, Dominik Schenten, and Esther Florsheim of Yale and the Howard Hughes Medical Institute.

The study was supported by grants from the National Institutes of Health (RO1 AI08977, 5RO1 AI055502, and R37 AI046688), and the Howard Hughes Medical Institute.

DOI: dx.doi.org/10.1016/j.immuni.2013.10.006

Source: Yale University
    
 
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