Human interleukin‐9 supports formation of a subpopulation of erythroid bursts that are responsive to interleukin‐3

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Abstract
We have investigated the biological activities of recombinant human interleukin‐9 (IL‐9) on enriched hematopoietic progenitors, alone or in combination with other cytokines, including Epo, G‐CSF, IL‐3, and GM‐CSF, under serum‐containing and serum‐free cultures. IL‐9 alone did not support colony formation. However, IL‐9 plus Epo induced erythroid burst (BFU‐E) formation derived from peripheral blood (PB) progenitors. Delayed addition experiments demonstrated that a part of bone marrow (BM) derived BFU‐E, which seems to be immature, only responded to IL‐9 and formed erythroid bursts. The burst‐promoting activity (BPA) of IL‐9 was confirmed using neutralizing aIL‐3, aGM‐CSF, and aIL‐9 antisera and serum‐free culture. IL‐9 supported a part of BFU‐E population that respond to IL‐3, which was almost identical to the number of BFU‐E supported by GM‐CSF. IL‐9 had no additive effect on erythroid and mixed colony formation supported by IL‐3. In contrast, IL‐9 showed an additive effect on erythroid burst formation supported by GM‐CSF in serum‐free culture. These data suggest that IL‐9 and GM‐CSF act on distinct IL‐3‐responsive BFU‐E population. In addition, delayed addition experiment clearly demonstrated that IL‐9 supports survival and the early stage of proliferation of BFU‐E. These results led us to propose that IL‐9 possibly acts as a BPA and selectively supports a subpopulation of early class of BFU‐E that respond to IL‐3.

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