King Ryan D, Lubinski John M, Friedman Harvey M
University of Pennsylvania, Philadelphia, 19104-6073, USA.
Arch Virol. 2009;154(4):609-18. doi: 10.1007/s00705-009-0351-7. Epub 2009 Mar 17.
Galectin-3 binds beta-galactoside-containing sugars and is a chemoattractant for monocytes, macrophages, and neutrophils. Galectin-3 was identified by mass spectrometry from an anti-gI affinity column; however, we determined that galectin-3 did not bind gI, but rather that HSV-1 infection increased galectin-3 binding to carbohydrate residues on IgG. Our conclusions are based on the following observations: (1) galectin-3 from cells infected with a gI-deleted HSV-1 mutant virus bound anti-gI IgG; (2) galectin-3 from wild-type HSV-1 infected cells bound nonimmune IgG; (3) more galectin-3 from infected than uninfected cells bound IgG; and (4) binding to IgG was blocked by lactose, a competitive inhibitor of galectin-3 carbohydrate binding. HSV-1 infection did not increase galectin-3 expression, but did increase its secretion. We propose that increased carbohydrate binding and secretion of galectin-3 contribute to an early pro-inflammatory innate immune response to HSV-1 infection.
半乳糖凝集素-3可结合含β-半乳糖苷的糖类，是单核细胞、巨噬细胞和中性粒细胞的趋化因子。通过质谱法从抗gI亲和柱中鉴定出半乳糖凝集素-3；然而，我们确定半乳糖凝集素-3不结合gI，而是单纯疱疹病毒1型（HSV-1）感染增加了半乳糖凝集素-3与IgG上碳水化合物残基的结合。我们的结论基于以下观察结果：（1）来自感染了缺失gI的HSV-1突变病毒的细胞的半乳糖凝集素-3结合抗gI IgG；（2）来自野生型HSV-1感染细胞的半乳糖凝集素-3结合非免疫IgG；（3）感染细胞中结合IgG的半乳糖凝集素-3比未感染细胞中的更多；（4）半乳糖凝集素-3碳水化合物结合的竞争性抑制剂乳糖可阻断与IgG的结合。HSV-1感染并未增加半乳糖凝集素-3的表达，但增加了其分泌。我们认为，半乳糖凝集素-3碳水化合物结合和分泌的增加有助于对HSV-1感染产生早期促炎性先天免疫反应。
