Type II interferon promotes differentiation of myeloid-biased hematopoietic stem cells.
Type II interferon promotes differentiation of myeloid-biased hematopoietic stem cells.
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DOI：
10.1002/stem.1799
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发表时间：
2014-11
期刊：
影响因子：
5.2
通讯作者：
King, Katherine Y.
中科院分区：
文献类型：
--
作者：
Matatall, Katie A.;Shen, Ching-Chieh;Challen, Grant A.;King, Katherine Y.
Interferon gamma (IFNγ) promotes cell division of hematopoietic stem cells (HSCs) without affecting the total HSC number. We postulated that IFNγ stimulates differentiation of HSCs as part of the innate immune response. Here we report that type II interferon signaling is required, both at baseline and during an animal model of LCMV infection, to maintain normal myeloid development. By separately evaluating myeloid-biased and lymphoid-biased HSC subtypes, we found that myeloid-biased HSCs express higher levels of IFNγ receptor and are specifically activated to divide after recombinant IFNγ exposure in vivo. HSCs show increased expression of the transcription factor C/EBPβ after infection. Furthermore, myeloid-biased HSCs are transiently depleted from the marrow during the Type II interferon-mediated immune response to Mycobacterium avium infection, as measured both functionally and phenotypically. These findings indicate that IFNγ selectively promotes differentiation of myeloid-biased HSCs during an innate immune response to infection. This represents the first report of a context and a mechanism for discriminate utilization of the alternate HSC subtypes. Terminal differentiation, at the expense of self-renewal, may compromise HSC populations during states of chronic inflammation.
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