Department of Anatomy, Physiology and Cell Biology, Center for Comparative Medicine, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616, USA.
J Immunol. 2012 Sep 1;189(5):2537-44. doi: 10.4049/jimmunol.1200429. Epub 2012 Jul 30.
Recent studies have shed light on the connection between elevated erythropoetin production/spleen erythropoiesis and increased susceptibility to Salmonella infection. In this article, we provide another mouse model, the SIRPα-deficient (Sirpα⁻/⁻) mouse, that manifests increased erythropoiesis as well as heightened susceptibility to Salmonella infection. Sirpα⁻/⁻ mice succumbed to systemic infection with attenuated Salmonella, possessing significantly higher bacterial loads in both the spleen and the liver. Moreover, Salmonella-specific Ab production and Ag-specific CD4 T cells were reduced in Sirpα⁻/⁻ mice compared with wild-type controls. To further characterize the potential mechanism underlying SIRPα-dependent Ag-specific CD4 T cell priming, we demonstrate that lack of SIRPα expression on dendritic cells results in less efficient Ag processing and presentation in vitro. Collectively, these findings demonstrate an indispensable role of SIRPα for protective immunity to Salmonella infection.
最近的研究揭示了红细胞生成素产生/脾脏红细胞生成增加与沙门氏菌感染易感性增加之间的联系。在本文中,我们提供了另一种小鼠模型,即 SIRPα 缺陷(Sirpα⁻/⁻)小鼠,该模型表现出红细胞生成增加以及对沙门氏菌感染的易感性增加。Sirpα⁻/⁻小鼠对减毒沙门氏菌的全身感染容易受到影响,其脾脏和肝脏中的细菌载量明显更高。此外,与野生型对照相比,Sirpα⁻/⁻小鼠的沙门氏菌特异性 Ab 产生和 Ag 特异性 CD4 T 细胞减少。为了进一步阐明 SIRPα 依赖性 Ag 特异性 CD4 T 细胞启动的潜在机制,我们证明树突状细胞上缺乏 SIRPα 表达会导致体外 Ag 处理和呈递效率降低。总的来说,这些发现表明 SIRPα 在保护性免疫抵抗沙门氏菌感染方面起着不可或缺的作用。