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CUTTING EDGE |
,
Departments of
*
Cell Biology, Neurobiology and Anatomy, and
Pathology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153;
Department of Hematopoiesis, American Red Cross, Rockville, MD 20855;
Department of Anatomy and Cell Biology, George Washington University Medical Center, Washington, DC 20037;
¶ Blood Research Institute, Blood Center of Southeast Wisconsin, and
|| Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, WI 53226
Both type-2 CD4+ Th cells (CD4+Th2) and type-2 innate effector cells play critical roles in generating type-2 immunity that can either be protective against parasitic infection or cause tissue damage in allergy and asthma. How innate effector cells acquire the capacity to produce Th2 cytokines is not entirely known. We previously showed that IL-4 induced differentiation of Th2 cytokine-producing eosinophils. To determine whether other Th2 cytokines can also induce Th2 cytokine-producing capacity in innate effector cells, we cultured bone marrow progenitor cells in the presence of various Th2 cytokines. IL-5, but not IL-13 or IL-25, primed bone marrow progenitor cells to differentiate into robust IL-4-producing cells. The majority of IL-4-producing cells induced by IL-5 were eosinophils. Importantly, IL-5 completely depended on STAT5 to promote IL-4-producing capacity in eosinophils. Thus, our study demonstrates that IL-5 functions as a potent factor that drives bone marrow progenitor cells into IL-4-producing eosinophils.
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