Institute of Biochemistry, Medical Faculty, University Leipzig, 04103 Leipzig, Germany.
J Biol Chem. 2011 Jan 21;286(3):2101-10. doi: 10.1074/jbc.M110.196659. Epub 2010 Nov 19.
The X-chromosomal GPR34 gene encodes an orphan G(i) protein-coupled receptor that is highly conserved among vertebrates. To evaluate the physiological relevance of GPR34, we generated a GPR34-deficient mouse line. GPR34-deficient mice were vital, reproduced normally, and showed no gross abnormalities in anatomical, histological, laboratory chemistry, or behavioral investigations under standard housing. Because GPR34 is highly expressed in mononuclear cells of the immune system, mice were specifically tested for altered functions of these cell types. Following immunization with methylated BSA, the number of granulocytes and macrophages in spleens was significantly lower in GPR34-deficient mice as in wild-type mice. GPR34-deficient mice showed significantly increased paw swelling in the delayed type hypersensitivity test and higher pathogen burden in extrapulmonary tissues after pulmonary infection with Cryptococcus neoformans compared with wild-type mice. The findings in delayed type hypersensitivity and infection tests were accompanied by significantly different basal and stimulated TNF-α, GM-CSF, and IFN-γ levels in GPR34-deficient animals. Our data point toward a functional role of GPR34 in the cellular response to immunological challenges.
X 染色体上的 GPR34 基因编码一个孤儿 G(i)蛋白偶联受体,在脊椎动物中高度保守。为了评估 GPR34 的生理相关性,我们构建了 GPR34 缺陷型小鼠品系。GPR34 缺陷型小鼠具有生命力,繁殖正常,在标准饲养条件下进行解剖学、组织学、实验室化学或行为学研究,未显示出明显的异常。由于 GPR34 在免疫系统的单核细胞中高度表达,因此特别测试了这些细胞类型的功能改变。在用甲基化 BSA 免疫后,GPR34 缺陷型小鼠脾脏中的粒细胞和巨噬细胞数量明显低于野生型小鼠。与野生型小鼠相比,GPR34 缺陷型小鼠在迟发型超敏反应试验中爪子肿胀明显增加,在新型隐球菌肺部感染后的肺外组织中病原体负担更高。迟发型超敏反应和感染试验中的发现伴随着 GPR34 缺陷型动物中基础和刺激的 TNF-α、GM-CSF 和 IFN-γ 水平的显著差异。我们的数据表明 GPR34 在免疫挑战的细胞反应中具有功能作用。