Sialic acids (Sias) on the B cell membrane are involved in cell migration, in the control of the complement system and, as sialic acid-binding immunoglobulin-like lectin (Siglec) ligands, in the regulation of cellular signaling. We studied the role of sialoglycans on B cells in a mouse model with B cell-specific deletion of cytidine monophosphate sialic acid synthase (CMAS), the enzyme essential for the synthesis of sialoglycans. Surprisingly, these mice showed a severe B cell deficiency in secondary lymphoid organs. Additional depletion of the complement factor C3 rescued the phenotype only marginally, demonstrating a complement-independent mechanism. The B cell survival receptor BAFF receptor was not up-regulated, and levels of activated caspase 3 and processed caspase 8 were high in B cells of Cmas-deficient mice, indicating ongoing apoptosis. Overexpressed Bcl-2 could not rescue this phenotype, pointing to extrinsic apoptosis. These results show that sialoglycans on the B cell surface are crucial for B cell survival by counteracting several death-inducing pathways.

中文翻译：

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B 细胞上的唾液酸对其生存至关重要，并可防止细胞凋亡。

B 细胞膜上的唾液酸 (Sias) 参与细胞迁移、补体系统的控制以及作为唾液酸结合免疫球蛋白样凝集素 (Siglec) 配体的细胞信号调节。我们研究了唾液酸聚糖对 B 细胞在 B 细胞特异性缺失胞苷单磷酸唾液酸合酶 (CMAS) 小鼠模型中的作用，CMAS 是合成唾液酸聚糖所必需的酶。令人惊讶的是，这些小鼠在次级淋巴器官中表现出严重的 B 细胞缺陷。补体因子 C3 的额外消耗仅略微挽救了表型，证明了补体独立机制。B 细胞存活受体 BAFF 受体没有上调，并且在 Cmas 缺陷小鼠的 B 细胞中活化的半胱天冬酶 3 和加工的半胱天冬酶 8 水平很高，表明正在进行的细胞凋亡。过度表达的 Bcl-2 无法挽救这种表型，表明存在外源性细胞凋亡。这些结果表明，B 细胞表面的唾液酸聚糖通过抵消几种死亡诱导途径，对 B 细胞存活至关重要。