Sialoadhesin-deficient mice exhibit subtle changes in B- and T-Cell populations and reduced immunoglobulin M levels
Sialoadhesin-deficient mice exhibit subtle changes in B- and T-Cell populations and reduced immunoglobulin M levels
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DOI：
10.1128/mcb.26.4.1549-1557.2006
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发表时间：
2006-02-01
影响因子：
5.3
通讯作者：
Crocker, PR
中科院分区：
文献类型：
--
作者：
Oetke, C;Vinson, MC;Crocker, PR
唾液粘附素（sialoadhesion in, Sn，也称为siglec1或CD169）是一种跨膜受体，是唾液酸结合免疫球蛋白样凝集素Siglec家族的原型成员。它在造血和淋巴组织中常驻巨噬细胞的特定亚群以及炎症巨噬细胞上表达。为了研究其功能，我们产生了sn缺陷小鼠，并通过荧光活化细胞分选分析和免疫组织化学证实这些小鼠是真正的null。缺乏So的小鼠可以存活和生育，没有发育异常。细胞群分析显示，在骨髓、腹腔和胸腺中没有差异，但在缺锡小鼠的脾脏和淋巴结中，CD8 T细胞少量增加，b220阳性细胞减少。此外，脾脏滤泡B细胞略有减少，边缘带B细胞数量增加。B细胞和t细胞的成熟以及对巯基乙酸盐刺激的反应仅受锡缺乏的轻微影响。免疫球蛋白M （IgM）滴度在sn缺陷小鼠中显著降低，但IgG亚类滴度相似。这些结果表明唾液黏附素的作用是调节免疫系统的细胞，而不是影响稳态造血。
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 So 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.