Baldridge等人利用一個(gè)關(guān)于細(xì)菌感染的小鼠模型發(fā)現(xiàn)，鳥分枝桿菌感染會(huì)對(duì)造血干細(xì)胞產(chǎn)生一個(gè)強(qiáng)大的刺激效應(yīng)，而且這種刺激是由γ-干擾素調(diào)控的,。
血液中的循環(huán)免疫細(xì)胞在感染中被消耗，而且這項(xiàng)工作表明,，骨髓中的原始干細(xì)胞在它們的替換中扮演一個(gè)角色,。
同時(shí)，這項(xiàng)工作對(duì)于在HIV/AIDS或肺結(jié)核等慢性感染過(guò)程中,、以及在骨髓移植恢復(fù)過(guò)程中將γ-干擾素用作一種治療藥物也有意義,。(生物谷Bioon.com)
生物谷推薦原文出處：
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.
