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

生理和病理条件下肠内淋巴细胞迁移的调节TECK/CCL 25在粘膜淋巴细胞粘附于小肠而不是在非炎症和炎症条件下的结肠中起重要作用。在对卵白蛋白慢性过敏的大鼠中，CD 4 T淋巴细胞通过MAdCAM-1依赖的过程在绒毛和派尔集合淋巴结中显著积聚。树突状细胞通过肠淋巴的迁移动力学分离的树突状细胞以时间依赖的方式在肠系膜淋巴结中积聚，在48 h时达到最大积聚。ICAM-1或CD 11b/c的抑制不影响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。肠系膜淋巴结中巨噬细胞的反应Parasinus巨噬细胞在淋巴结的瞬时抗转移能力中起作用，在转移早期这些细胞分泌的细胞因子增加。细胞因子诱导的恶化可能是随后癌症增殖的原因。巨噬细胞移动抑制因子在癌细胞中表达，可调节细胞因子反应和巨噬细胞的移动。

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.