The Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
PLoS One. 2013;8(3):e60124. doi: 10.1371/journal.pone.0060124. Epub 2013 Mar 29.
The migration of lymphocytes to the small intestine is controlled by expression of the integrin α4β7 and the chemokine receptor CCR9. However, the molecules that specifically regulate migration to the large intestine remain unclear. Immunity to infection with the large intestinal helminth parasite Trichuris muris is dependent upon CD4(+) T cells that migrate to the large intestine. We examine the role of specific chemokine receptors, adhesion molecules and glycosyltransferases in the development of protective immunity to Trichuris. Mice deficient in expression of the chemokine receptors CCR2 or CCR6 were resistant to infection with Trichuris. Similarly, loss of CD34, CD43, CD44 or PSGL-1 had no effect on resistance to infection. In contrast, simultaneous deletion of the Core2 β1,6-N-acetylglucosaminyltransferase (C2GnT) enzymes C2GnT1 and C2Gnt2 resulted in delayed expulsion of worms. These results suggest that C2GnT-dependent modifications may play a role in migration of protective immune cells to the large intestine.
淋巴细胞迁移到小肠受整合素 α4β7 和趋化因子受体 CCR9 的表达控制。然而，特异性调节向大肠迁移的分子尚不清楚。对大肠寄生虫旋毛虫感染的免疫依赖于迁移到大肠的 CD4(+) T 细胞。我们研究了特定趋化因子受体、黏附分子和糖基转移酶在旋毛虫保护性免疫中的作用。表达趋化因子受体 CCR2 或 CCR6 缺陷的小鼠对旋毛虫感染具有抗性。同样，缺乏 CD34、CD43、CD44 或 PSGL-1 对感染的抵抗力没有影响。相比之下，同时缺失 Core2 β1,6-N-乙酰氨基葡萄糖基转移酶 (C2GnT) 酶 C2GnT1 和 C2Gnt2 导致蠕虫排出延迟。这些结果表明 C2GnT 依赖性修饰可能在保护性免疫细胞向大肠迁移中发挥作用。
