Baldridge等人利用一个关于细菌感染的小鼠模型发现，鸟分枝杆菌感染会对造血干细胞产生一个强大的刺激效应，而且这种刺激是由γ-干扰素调控的。
血液中的循环免疫细胞在感染中被消耗，而且这项工作表明，骨髓中的原始干细胞在它们的替换中扮演一个角色。
同时，这项工作对于在HIV/AIDS或肺结核等慢性感染过程中、以及在骨髓移植恢复过程中将γ-干扰素用作一种治疗药物也有意义。(生物谷Bioon.com)
生物谷推荐原文出处：
Nature doi:10.1038/nature09135
Quiescent haematopoietic stem cells are activated by IFN-γ in response to chronic infection
Megan T. Baldridge,Katherine Y. King,Nathan C. Boles,David C. Weksberg& Margaret A. Goodell
Lymphocytes and neutrophils are rapidly depleted by systemic infection1. Progenitor cells of the haematopoietic system, such as common myeloid progenitors and common lymphoid progenitors, increase the production of immune cells to restore and maintain homeostasis during chronic infection, but the contribution of haematopoietic stem cells (HSCs) to this process is largely unknown2. Here we show, using an in vivo mouse model of Mycobacterium avium infection, that an increased proportion of long-term repopulating HSCs proliferate during M. avium infection, and that this response requires interferon-γ (IFN-γ) but not interferon-α (IFN-α) signalling. Thus, the haematopoietic response to chronic bacterial infection involves the activation not only of intermediate blood progenitors but of long-term repopulating HSCs as well. IFN-γ is sufficient to promote long-term repopulating HSC proliferation in vivo; furthermore, HSCs from IFN-γ-deficient mice have a lower proliferative rate, indicating that baseline IFN-γ tone regulates HSC activity. These findings implicate IFN-γ both as a regulator of HSCs during homeostasis and under conditions of infectious stress. Our studies contribute to a deeper understanding of haematological responses in patients with chronic infections such as HIV/AIDS or tuberculosis3, 4, 5.
