胶原蛋白沉积在通过损害次级淋巴器官微环境来消耗CD4+ T细胞以及限制HIV-1和SIV感染中的重建方面所起的作用。
The role of collagen deposition in depleting CD4+ T cells and limiting reconstitution in HIV-1 and SIV infections through damage to the secondary lymphoid organ niche.
作者信息
Estes Jacob D, Haase Ashley T, Schacker Timothy W
机构信息
AIDS and Cancer Virus Program, Science Applications International Corporation-Frederick, Inc., National Cancer Institute, Frederick, MD, USA.
出版信息
Semin Immunol. 2008 Jun;20(3):181-6. doi: 10.1016/j.smim.2008.04.002. Epub 2008 Jul 2.
Abstract
The hallmark of HIV/SIV infections is the progressive depletion of CD4+ T cells that ultimately renders the host incapable of defending against AIDS defining opportunistic infections and malignancies. Although many potential mechanisms have been proposed to explain CD4+ T cell loss, we review here the growing evidence that fibrotic 'scarring' and consequent damage to the lymphatic tissue niche contributes to CD4+ T cell decline and limits CD4+ T cell re-population with retroviral therapy.
摘要
HIV/SIV感染的标志是CD4+ T细胞逐渐耗竭，最终使宿主无法抵御导致艾滋病的机会性感染和恶性肿瘤。尽管已经提出了许多潜在机制来解释CD4+ T细胞的损失，但我们在此回顾越来越多的证据表明，纤维化“瘢痕形成”以及随之而来的对淋巴组织微环境的损害导致CD4+ T细胞数量下降，并限制了逆转录病毒疗法后CD4++ T细胞的重新增殖。
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