Katayama H, Kitagawa S, Masuyama J, Yaoita H
Department of Dermatology, Jichi Medical School, Tochigi-ken, Japan.
J Invest Dermatol. 1991 Nov;97(5):949-52. doi: 10.1111/1523-1747.ep12491818.
In an in vitro study, intended to develop tumoricidal therapy with the use of human leukocyte, an interesting phenomenon was found. Normal human polymorphonuclear leukocytes (PMN) plated on a cell line established from malignant trichilemmal cyst (DJM-1), a kind of squamous cell carcinoma, in a serum-free media and incubated for 48 h induced the detachment of DJM-1. The detachment was more extensive as the number of PMN increased. The detachment rate was 97.0% when the number of PMN and DJM-1 in a well was in a ratio 2.4:1 and the viability of detached DJM-1 was 96.5%. Two kinds of proteinase inhibitors, especially the inhibitor of neutrophil elastase, fetal bovine serum, and monoclonal anti-laminin antibody inhibited the detachment significantly. Furthermore, when PMN were seeded in a chamber with a filter membrane bottom to prevent direct contact with DJM-1, DJM-1 detachment decreased to 14.2%. In view of these results, the following mechanism was postulated. Activated by their adhesion to DJM-1, especially between laminin receptor on PMN and laminin on DJM-1, PMN secreted proteinases, resulting in DJM-1 detachment. This phenomenon might be an expression of cytotoxicity of PMN to cancer cells, because cultured cancer cells of epithelium origin such as DJM-1 can grow only after they are firmly attached to the substratum. This phenomenon, in turn, may explain the final step in the induction of epidermal-dermal separation in subepidermal bullous diseases with PMN infiltration such as bullous pemphigoid and dermatitis herpetiformis if we could regard DJM-1 as normal keratinocyte.
在一项旨在开发利用人白细胞进行肿瘤杀伤治疗的体外研究中,发现了一个有趣的现象。将正常人多形核白细胞(PMN)接种于由恶性毛囊囊肿(DJM-1)建立的细胞系上,DJM-1是一种鳞状细胞癌,在无血清培养基中培养48小时后,可诱导DJM-1细胞脱落。随着PMN数量的增加,细胞脱落更为广泛。当孔中PMN与DJM-1的数量比为2.4:1时,脱落率为97.0%,脱落的DJM-1细胞活力为96.5%。两种蛋白酶抑制剂,尤其是中性粒细胞弹性蛋白酶抑制剂、胎牛血清和抗层粘连蛋白单克隆抗体可显著抑制细胞脱落。此外,当将PMN接种于带有滤膜底部的小室中以防止与DJM-1直接接触时,DJM-1的脱落率降至14.2%。基于这些结果,推测了以下机制。PMN通过与DJM-1粘附而被激活,尤其是PMN上的层粘连蛋白受体与DJM-1上的层粘连蛋白之间的粘附,导致PMN分泌蛋白酶,从而引起DJM-1细胞脱落。这种现象可能是PMN对癌细胞细胞毒性的一种表现,因为像DJM-1这样的上皮来源的培养癌细胞只有在牢固附着于基质后才能生长。反过来,如果我们将DJM-1视为正常角质形成细胞,这种现象可能解释了在伴有PMN浸润的表皮下大疱性疾病如大疱性类天疱疮和疱疹样皮炎中表皮-真皮分离诱导的最后步骤。