Bhattacharya Deepta, Rossi Derrick J, Bryder David, Weissman Irving L
Department of Pathology, Institute of Cancer and Stem Cell Biology and Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
J Exp Med. 2006 Jan 23;203(1):73-85. doi: 10.1084/jem.20051714. Epub 2005 Dec 27.
In the absence of irradiation or other cytoreductive conditioning, endogenous hematopoietic stem cells (HSCs) are thought to fill the unique niches within the bone marrow that allow maintenance of full hematopoietic potential and thus prevent productive engraftment of transplanted donor HSCs. By transplantation of purified exogenous HSCs into unconditioned congenic histocompatible strains of mice, we show that approximately 0.1-1.0% of these HSC niches are available for engraftment at any given point and find no evidence that endogenous HSCs can be displaced from the niches they occupy. We demonstrate that productive engraftment of HSCs within these empty niches is inhibited by host CD4+ T cells that recognize very subtle minor histocompatibility differences. Strikingly, transplantation of purified HSCs into a panel of severe combined immunodeficient (SCID) mice leads to a rapid and complete rescue of lymphoid deficiencies through engraftment of these very rare niches and expansion of donor lymphoid progenitors. We further demonstrate that transient antibody-mediated depletion of CD4+ T cells allows short-term HSC engraftment and regeneration of B cells in a mouse model of B(-) non-SCID. These experiments provide a general mechanism by which transplanted HSCs can correct hematopoietic deficiencies without any host conditioning or with only highly specific and transient lymphoablation.
在没有辐射或其他细胞减灭预处理的情况下,内源性造血干细胞(HSC)被认为占据了骨髓内独特的微环境,这些微环境能够维持完全的造血潜能,从而阻止移植的供体HSC有效植入。通过将纯化的外源性HSC移植到未经预处理的同基因组织相容性小鼠品系中,我们发现,在任何给定时间点,约0.1 - 1.0%的这些HSC微环境可用于植入,且没有证据表明内源性HSC能够从它们所占据的微环境中被取代。我们证明,识别非常细微的次要组织相容性差异的宿主CD4 + T细胞会抑制HSC在这些空的微环境中的有效植入。引人注目的是,将纯化的HSC移植到一组严重联合免疫缺陷(SCID)小鼠中,通过植入这些非常罕见的微环境和供体淋巴祖细胞的扩增,可迅速且完全地挽救淋巴缺陷。我们进一步证明,在B(-)非SCID小鼠模型中,短暂的抗体介导的CD4 + T细胞耗竭可使HSC短期植入并使B细胞再生。这些实验提供了一种通用机制,通过该机制,移植的HSC无需任何宿主预处理或仅通过高度特异性和短暂的淋巴细胞清除就能纠正造血缺陷。