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Researchers from Cincinnati Children’s and Tel Aviv
University in Israel have discovered a molecular pathway that has broad
implications for treating eosinophil-associated disorders.
Eosinophils are normal cellular components of blood, but
when the body produces too many eosinophils it can cause chronic inflammation
resulting in tissue damage, often in the gastrointestinal system. Eosinophils
are regulated by interleukin 5 (IL-5), a protein that triggers them to leave
the bone marrow and enter the bloodstream.
The new research identifies a pathway for counterbalancing
what happens when IL-5 triggers eosinophils. The study is published online in the journal Nature Immunology.
"The fundamental knowledge we have gained may one day
yield new therapies to treat devastating eosinophilic disorders," says
Ariel Munitz, PhD, a researcher at the Sackler School of Medicine at Tel Aviv
University and corresponding author of the study.
Munitz and Marc Rothenberg, MD, PhD, director of Allergy and Immunology at Cincinnati Children's, report that the newly identified pathway
involves a pair of proteins, PIR-A and PIR-B, that play a critical role in
eosinophil development. PIR-A induces eosinophils to die but PIR-B inhibits its
actions. For PIR-A to keep eosinophil production in check, PIR-B must be shut
Asthmatic mice bred to lack PIR-B had little expansion of
eosinophils in their blood and less asthmatic inflammation in their lungs than
normal mice. This finding indicates that inflammation might be better
controlled by enhancing PIR-A or weakening PIR-B so that it inhibits PIR-A to a
The study is part of the Israel Exchange Program (IEP) at
Cincinnati Children's, a collaborative effort with leading Israeli institutions
to improve clinical care, train clinicians and researchers and accelerate
development of technological breakthroughs that benefit children.
Rothenberg, MD, PhD, director of Allergy and Immunology at Cincinnati
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