MECHANISM OF REGULATING MOBILIZATION AND MIGRATION OF ANTIGEN PRESENTING CELLS DURING INFLAMMATION

在生理和病理条件下，TECK/CCL25在粘膜淋巴细胞与小肠的黏附中起重要作用，但在单火和炎症条件下对结肠的黏附不起重要作用。慢性卵蛋白过敏大鼠绒毛和Peyer‘S斑块中CD4T细胞通过MAdCAM1依赖的过程显著聚集。树突状细胞通过肠淋巴的迁移动力学：分离的树突状细胞在肠系膜淋巴结中以时间依赖的方式聚集，48h达到最大聚集，抑制细胞间黏附分子-1或CD11b/c不影响DC迁移。树突状细胞的迁移能力与其成熟程度密切相关，不同的趋化因子/趋化因子受体的使用可能是树突状细胞通过肠淋巴迁移动力学的主要调节因素。肠系膜淋巴结内巨噬细胞的反应副内脏巨噬细胞在结节的瞬时抗转移能力中发挥作用，这些细胞在转移的早期阶段分泌的细胞因子增加。细胞因子诱导的恶化可能是随后的癌症增殖的原因。巨噬细胞移动抑制因子在癌细胞中的表达可能调节巨噬细胞的细胞因子反应和迁移。

Regulation of lymphocyte migration in the intestine under physiological and pathological conditionTECK/CCL25 plays an important role in the adherence of mucosal lymphocytes to the small intestine but not the colon under uniflamed as well as inflamed conditions. CD4T lymphocytes significantly accumulated in villus as well as in Peyer' s patches via a MAdCAM-1-dependent process in rats with a chronic allergy to ovalbumin.Migration kinetics of dendritic cells via intestinal lymphThe isolated dendritic cells accumulated in mesenteric lymph nodes in a time-dependent manner with maximal accumulation at 48 h. Inhibition of ICAM-1 or CD11b/c did not affect DC migration. The migratory ability of dendritic cells correlates well with their degree of maturation, and different chemokine/chemokine receptor usage may be the main regulator of dendritic cell migration kinetics through intestinal lymph.Response of macrophage in mesenteric lymph nodeParasinus macrophages play a role in the transient anti-metastatic capability of the node, and cytokines secreted by these cells increased at the early stages of metastasis. Deterioration of cytokine induction may be responsible for subsequent cancer proliferation. Macrophage migration inhibitory factor expressed in the cancer cells may modulate cytokine responses and migration of the macrophages.