Li Shuai, Dislich Bastian, Brakebusch Cord H, Lichtenthaler Stefan F, Brocker Thomas
Institute for Immunology, Ludwig-Maximilians-University, 80336 Munich, Germany;
German Center for Neurodegenerative Diseases, 81377 Munich, Germany;
J Immunol. 2015 Nov 1;195(9):4244-56. doi: 10.4049/jimmunol.1500676. Epub 2015 Sep 25.
Tissues accommodate defined numbers of dendritic cells (DCs) in highly specific niches where different intrinsic and environmental stimuli control DC life span and numbers. DC homeostasis in tissues is important, because experimental changes in DC numbers influence immunity and tolerance toward various immune catastrophes and inflammation. However, the precise molecular mechanisms regulating DC life span and homeostasis are unclear. We report that the GTPase RhoA controls homeostatic proliferation, cytokinesis, survival, and turnover of cDCs. Deletion of RhoA strongly decreased the numbers of CD11b(-)CD8(+) and CD11b(+)Esam(hi) DC subsets, whereas CD11b(+)Esam(lo) DCs were not affected in conditional RhoA-deficient mice. Proteome analyses revealed a defective prosurvival pathway via PI3K/protein kinase B (Akt1)/Bcl-2-associated death promoter in the absence of RhoA. Taken together, our findings identify RhoA as a central regulator of DC homeostasis, and its deletion decreases DC numbers below critical thresholds for immune protection and homeostasis, causing aberrant compensatory DC proliferation.
组织在高度特异性的微环境中容纳特定数量的树突状细胞(DC),在这些微环境中,不同的内在和环境刺激控制着DC的寿命和数量。组织中的DC稳态很重要,因为DC数量的实验性变化会影响对各种免疫灾难和炎症的免疫和耐受性。然而,调节DC寿命和稳态的精确分子机制尚不清楚。我们报告,GTP酶RhoA控制cDC的稳态增殖、胞质分裂、存活和更新。RhoA的缺失强烈降低了CD11b(-)CD8(+)和CD11b(+)Esam(hi)DC亚群的数量,而在条件性RhoA缺陷小鼠中,CD11b(+)Esam(lo)DC不受影响。蛋白质组分析显示,在没有RhoA的情况下,通过PI3K/蛋白激酶B(Akt1)/Bcl-2相关死亡促进因子的促存活途径存在缺陷。综上所述,我们的研究结果确定RhoA是DC稳态的核心调节因子,其缺失会使DC数量降至免疫保护和稳态的临界阈值以下,导致异常的代偿性DC增殖。