Department of Dermatology, Venerology and Allergology, Universitätsklinikum Leipzig, Leipzig, Germany.
Department of Environmental Immunology, UFZ - Helmholtz Centre for Environmental Research Leipzig-Halle, Leipzig, Germany.
Exp Dermatol. 2017 Nov;26(11):1060-1067. doi: 10.1111/exd.13374. Epub 2017 Aug 29.
In human dendritic cells (DCs), we previously demonstrated in vitro that syndecan-1 (SDC1) is downregulated during maturation correlating with enhanced motility. We investigated the effects of SDC1 on DC migration in vivo during TNCB(2,4,6-trinitro-1-chlorobenzene)-induced cutaneous hypersensitivity reaction (CHS) in mice. We show that DC in SDC1-deficient mice migrated faster and at a higher rate to lymph nodes draining the hapten-painted skin. Adoptive transfer of SDC1-deficient hapten- and fluorochrome-labelled DC into wild-type (WT) mice led to increased and faster migration of DC to paracortical lymph nodes, and to a stronger CHS compared to WT DC. In SDC1-/- mice, CCR7 remains longer on the DC surface within the first 15-minutes maturation (after LPS-induced maturation). In addition, a time-dependent upregulation of CCL2, CCL3, VCAM1 and talin was found during maturation in SDC1-/- DC. However, no difference in T-cell-stimulating capacity of SDC1-deficient DC was found compared to WT DC. Mechanistically, SDC1-deficient DC showed enhanced migration towards CCL21 and CCL19. This may result from functional overexpression of CCR7 in SDC1-/- DC. Increased and accelerated migration of otherwise functionally intact SDC1-deficient DC leads to an exacerbated CHS. Based on our results, we conclude that SDC1 on DC negatively regulates DC migration.
在人类树突状细胞 (DC) 中,我们之前在体外证明,syndecan-1 (SDC1) 在成熟过程中下调,与增强的迁移能力相关。我们研究了 SDC1 在小鼠 TNCB(2,4,6-三硝基-1-氯苯)诱导的皮肤超敏反应 (CHS) 过程中对 DC 体内迁移的影响。我们发现,SDC1 缺陷型小鼠中的 DC 迁移速度更快,迁移率更高,迁移到引流变应原涂抹皮肤的淋巴结。将 SDC1 缺陷型变应原和荧光染料标记的 DC 过继转移到野生型 (WT) 小鼠中,导致 DC 更快地迁移到副皮质淋巴结,并导致更强的 CHS,与 WT DC 相比。在 SDC1-/- 小鼠中,CCR7 在 LPS 诱导成熟后最初的 15 分钟内(成熟后)在 DC 表面停留时间更长。此外,在 SDC1-/- DC 的成熟过程中发现 CCL2、CCL3、VCAM1 和 talin 呈时间依赖性上调。然而,与 WT DC 相比,SDC1 缺陷型 DC 的 T 细胞刺激能力没有差异。从机制上讲,SDC1 缺陷型 DC 向 CCL21 和 CCL19 的迁移增强。这可能是由于 SDC1-/- DC 中 CCR7 的功能过表达。否则功能完整的 SDC1 缺陷型 DC 的增加和加速迁移导致 CHS 加剧。基于我们的结果,我们得出结论,SDC1 在 DC 上负调节 DC 迁移。