Center for Lung Biology, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, WA, USA.
Cell Cycle. 2010 Dec 15;9(24):4922-30. doi: 10.4161/cc.9.24.14209.
We recently described a new adhesion pathway in lymphocytes that is dependent on Cyclin-dependent kinase (Cdk) 4 activity and mediates lymphocyte interactions with endothelial matrix. We showed that Cdk4(-/-) mice had impaired recruitment of lymphocytes following bleomycin model of acute lung injury. In this study, we characterized the development and function of hematopoietic cells in Cdk4(-/-) mice and assessed the response of Cdk4(-/-) mice to allergen challenge. Cdk4(-/-) mice had hypoplastic thymuses with decreased total thymocyte cell numbers and increased CD4/CD8 double negative cells. Cdk4(-/-) bone marrow (BM) chimeric mice showed similar findings. Thymocytes from either Cdk4(-/-) or Cdk4(-/-) BM chimeric mice proliferated equally well as wild type controls in response to IL-2 activation. However Cdk4(-/-) thymocytes had decreased adhesion to both endothelial cell matrix and fibronectin compared to wildtype (WT) controls, whereas Cdk4(-/-) and WT splenocytes had similar adhesion. When Cdk4(-/-) BM chimeric mice and wild type BM chimeric mice were sensitized and challenged by intranasal administration of ovalbumin, we found no differences in allergic responses in the lung and airways between the two groups, as measured by inflammatory cell infiltrate, airway hyperreactivity, IgE levels and cytokine levels. In summary, we show that Cdk4 plays a previously unrecognized role in thymocyte maturation and adhesion, but is not required for thymocyte proliferation. In addition, Cdk4 is not required for lymphocyte trafficking to the lung following allergen sensitization and challenge.
我们最近描述了淋巴细胞中的一种新的黏附途径,该途径依赖于细胞周期蛋白依赖性激酶(Cdk)4 的活性,并介导淋巴细胞与内皮基质的相互作用。我们表明,在博来霉素诱导的急性肺损伤模型中,Cdk4(-/-)小鼠的淋巴细胞募集受损。在这项研究中,我们描述了 Cdk4(-/-)小鼠中造血细胞的发育和功能,并评估了 Cdk4(-/-)小鼠对变应原挑战的反应。Cdk4(-/-)小鼠的胸腺发育不良,总胸腺细胞数量减少,CD4/CD8 双阴性细胞增多。Cdk4(-/-)骨髓(BM)嵌合小鼠也表现出类似的发现。来自 Cdk4(-/-)或 Cdk4(-/-)BM 嵌合小鼠的胸腺细胞在对 IL-2 激活的反应中与野生型对照一样良好地增殖。然而,与野生型(WT)对照相比,Cdk4(-/-)胸腺细胞与内皮细胞基质和纤连蛋白的黏附减少,而 Cdk4(-/-)和 WT 脾细胞的黏附相似。当 Cdk4(-/-)BM 嵌合小鼠和野生型 BM 嵌合小鼠通过鼻内给予卵清蛋白致敏和挑战时,我们发现两组之间在肺部和气道中的过敏反应没有差异,如炎症细胞浸润、气道高反应性、IgE 水平和细胞因子水平。总之,我们表明 Cdk4 在胸腺细胞成熟和黏附中发挥了以前未被认识到的作用,但不是胸腺细胞增殖所必需的。此外,Cdk4 对于变应原致敏和挑战后淋巴细胞向肺部的迁移也不是必需的。