期刊
JOURNAL OF IMMUNOLOGY
卷 182, 期 5, 页码 2835-2841出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0802870
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类别
资金
- National Institutes of Health [R01 AI48568, R01 AI068083, R01 HL073284, R01 AI079087]
- Scholar Award from the Leukemia & Lymphoma Society [R01DK059380]
Recent work has established important roles for basophils in regulating immune responses. To exert their biological functions, basophils need to be expanded to critical numbers. However, the mechanisms underlying basophil expansion remain unclear. In this study, we established that IL-3 played an important role in the rapid and specific expansion of basophils. We found that the IL-3 complex (IL-3 plus anti-IL-3 Ab) greatly facilitated the differentiation of GMPs into basophil lineage-restricted progenitors (BaPs) but not into eosinophil lineage-restricted progenitors or most cells in the bone marrow. We also found that the IL-3 complex treatment resulted in similar to 4-fold increase in the number of basophil/mast cell progenitors (BMCPs) in the spleen. IL-3-driven basophil expansion depended on STAT5 signaling. We showed that GMPs but not common myeloid progenitors expressed low levels of HA receptor. IL-3 receptor expression was dramatically up-regulated in BaPs but not eosinophil lineage-restricted progenitors. Approximately 38% of BMCPS expressed the IL-3R alpha-chain. The up-regulated IL-3 receptor expression was not affected by HA or STAT5. Our findings demonstrate that HA induced specific expansion of basophils by directing GMPs to differentiate into BaPs in the bone marrow and by increasing the number of BMCPs in the spleen. The Journal of Immunology, 2009,182: 2835-2841.
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