Oetke Cornelia, Vinson Mary C, Jones Claire, Crocker Paul R
The Wellcome Trust Biocentre, School of Life Sciences, University of Dundee, Dow Street, Dundee DD1 5EH, United Kingdom.
Mol Cell Biol. 2006 Feb;26(4):1549-57. doi: 10.1128/MCB.26.4.1549-1557.2006.
Sialoadhesin (Sn, also called Siglec-1 or CD169) is a transmembrane receptor and the prototypic member of the Siglec family of sialic acid binding immunoglobulin-like lectins. It is expressed on specialized subsets of resident macrophages in hematopoietic and lymphoid tissues and on inflammatory macrophages. In order to investigate its function, we generated Sn-deficient mice and confirmed that these mice are true nulls by fluorescence-activated cell sorter analysis and immunohistochemistry. Mice deficient in Sn were viable and fertile and showed no developmental abnormalities. Analysis of cell populations revealed no differences in bone marrow, peritoneal cavity, and thymus, but there was a small increase in CD8 T cells and a decrease in B220-positive cells in spleens and lymph nodes of Sn-deficient mice. Furthermore, in spleen there was a slight decrease in follicular B cells with an increase in numbers of marginal zone B cells. B- and T-cell maturation as well as responses to stimulation with thioglycolate were only slightly affected by Sn deficiency. Immunoglobulin titers in Sn-deficient mice were significantly decreased for immunoglobulin M (IgM) but similar for IgG subclasses. These results suggest a role for sialoadhesin in regulating cells of the immune system rather than in influencing steady-state hematopoiesis.
唾液酸黏附素(Sn,也称为Siglec-1或CD169)是一种跨膜受体,也是唾液酸结合免疫球蛋白样凝集素Siglec家族的原型成员。它在造血组织和淋巴组织中的驻留巨噬细胞的特定亚群以及炎性巨噬细胞上表达。为了研究其功能,我们培育了Sn基因缺陷小鼠,并通过荧光激活细胞分选分析和免疫组织化学证实这些小鼠为真正的基因敲除小鼠。Sn基因缺陷小鼠能够存活且可育,未表现出发育异常。细胞群体分析显示,骨髓、腹腔和胸腺无差异,但Sn基因缺陷小鼠脾脏和淋巴结中的CD8 T细胞略有增加,B220阳性细胞减少。此外,脾脏中滤泡B细胞略有减少,边缘区B细胞数量增加。Sn基因缺陷对B细胞和T细胞的成熟以及对巯基乙酸刺激的反应仅产生轻微影响。Sn基因缺陷小鼠的免疫球蛋白M(IgM)滴度显著降低,但IgG亚类的滴度相似。这些结果表明唾液酸黏附素在调节免疫系统细胞方面发挥作用,而非影响稳态造血。