Analysis of Langerhans cell chemotactic factors

朗格汉斯细胞趋化因子分析

• 批准号: 07457189
• 负责人: NISHIOKA Kiyoshi
• 金额: $ 4.42万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1997
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07457189/
• 关键词: Langerhans cells; Chemstoctic fator; ytokine; Kernikine; Adhesion moleailes; Contat allergy; 培養因子; Langerhans Cell; 遊走; Cytokine; IL-4; TNF-α; 接触皮膚炎; ハプテン; T細胞; ケラチノサイト; リンパ節

1) In order to determine whether lymphnode (LN) cells can generate chemotactic factors, we investigated the chemotactic factor in the culture supernatant of LN cells obtained from sensitized mice by using a modified Boyden chamber methods.The chemotactic facotr appered in the culture supernatant at 24 h after haptenpainting. Antibodies againt both ICAM-1 and LFA-1 partially inhibited the chemotactic activity, but this was not case with anti-TNF-a mAb and anti-GM-CSF mAb. The molecules was heat labile and appeared as a molecules of 45-68 kDa. These results suggest that LN cellsa generated one of the chemotactic molecules of LC,which migrate to the regional LN in contact sensitivity.2) To clarify the further mechanism of the migration of LC from epidermis to lymph node, we investigeted the migration activities of murine LC to wards several cytokines and chemokines in vitro.We used modified Boyden chamber method and counted dendritic cells migrated to the lowere chamber as LC.In our system, migration of murine LC was stimulated by YNF-a, RANTES and MCP-1, but not by GM-CSF,IL-1b, IL-4 and IL-6.These data comfirm that TNF-a, RANTES and MCP-1 induced LC migration from epidermis during contact sensitization.3) We investigate the modulation of in vitro migratory activity of human epidermal Langerhans cells (LC) by T helper type 1 cells (Th1) and Th2 type cytokines. These data indicate that IL-4 secreted by T helper type 2 cells has a possibility to inhibit the LC migration induced by TNF-alpha or GM-CSF by the modulations of the expression of the adhesion molecules on human LC.

1)为探讨淋巴结（LN）细胞能否产生趋化因子，我们用改良的Boyden小室法检测了致敏小鼠LN细胞培养上清中的趋化因子，半抗原涂染后24 h培养上清中出现趋化因子。抗ICAM-1和LFA-1的单抗可部分抑制趋化活性，而抗TNF-α和抗GM-CSF的单抗则无此作用。该分子是热不稳定的，并且表现为45-68 kDa的分子。这些结果表明，LN细胞a产生的LC的趋化分子之一，迁移到局部LN的接触敏感性。2）为了阐明LC从表皮迁移到淋巴结的进一步机制，我们用改良的Boyden小室法，观察了小鼠LC对几种细胞因子和趋化因子的体外迁移活性，并将迁移到下小室的树突状细胞计数为LC，在我们的实验中，结果表明，TNF-α、RANTES和MCP-1能促进小鼠表皮细胞的迁移，而GM-CSF、IL-1b、IL-4和IL-6对小鼠表皮细胞的迁移无明显影响，提示TNF-α、RANTES和MCP-1在接触致敏过程中可诱导小鼠表皮细胞的迁移。这些数据表明，由T辅助2型细胞分泌的IL-4有可能通过调节人LC上粘附分子的表达来抑制TNF-α或GM-CSF诱导的LC迁移。

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