Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
PLoS One. 2011;6(10):e24431. doi: 10.1371/journal.pone.0024431. Epub 2011 Oct 3.
In addition to its complement-regulating activity, CD55 is a ligand of the adhesion class G protein-coupled receptor CD97; however, the relevance of this interaction has remained elusive. We previously showed that mice lacking a functional CD97 gene have increased numbers of granulocytes.
METHODOLOGY/RESULTS: Here, we demonstrate that CD55-deficient mice display a comparable phenotype with about two-fold more circulating granulocytes in the blood stream, the marginated pool, and the spleen. This granulocytosis was independent of increased complement activity. Augmented numbers of Gr-1-positive cells in cell cycle in the bone marrow indicated a higher granulopoietic activity in mice lacking either CD55 or CD97. Concomitant with the increase in blood granulocyte numbers, Cd55⁻/⁻ mice challenged with the respiratory pathogen Streptococcus pneumoniae developed less bacteremia and died later after infection.
Collectively, these data suggest that complement-independent interaction of CD55 with CD97 is functionally relevant and involved in granulocyte homeostasis and host defense.
除了具有补体调节活性外，CD55 还是黏附类 G 蛋白偶联受体 CD97 的配体；然而，这种相互作用的相关性仍不清楚。我们之前的研究表明，缺乏功能性 CD97 基因的小鼠粒细胞数量增加。
方法/结果：在这里，我们证明 CD55 缺陷型小鼠表现出类似的表型，其循环中的粒细胞数量在血液、边缘池和脾脏中增加了约两倍。这种粒细胞增多与补体活性的增加无关。骨髓中 Gr-1 阳性细胞处于细胞周期的比例增加表明，缺乏 CD55 或 CD97 的小鼠的粒状造血活性更高。与血液中粒细胞数量增加相一致的是，呼吸道病原体肺炎链球菌感染的 Cd55⁻/⁻ 小鼠发生菌血症的情况较少，感染后死亡时间较晚。
综上所述，这些数据表明 CD55 与 CD97 的补体非依赖性相互作用具有功能相关性，并参与粒细胞的稳态和宿主防御。
