Therole of 55 kDa and 75 kDa TNF receptor in sigraling of humen neutrophil

55 kDa和75 kDa TNF受体在人中性粒细胞信号传导中的作用

• 批准号: 06671210
• 负责人: OSUKA Yo
• 金额: $ 1.34万
• 依托单位: Ehime University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06671210/
• 关键词: TNF; lymphotoxin; TNF receptor; neutrophils; 腫瘍壊死因子レセプター; 生物活性

The expression and biological role of 55- and 75-kDa tumor necrosis factor-receptors (TNF-R) in human polymorphonuclear cells (PMN) in vitro were studied using agonistic rabbit polyclonal anti-TNF-R antibodies. PMN express 75-kDa TNF-R predominantly according to flow cytometric analysis and a ^<125>I-LT binding assay. PMN produce and release the superoxide anion on stimulation by human recombinant lymphotoxin (LT) in vitro. Anti-55- but not anti-75-kDa TNF-R antibody stimulated the superoxide release mimicking LT.Release of the elastase from azurophilic granule of PMN was augmented by LT in vitro. Anti-55- but not anti-75-kDa TNF-R antibody augmented the clastase release mimicking LT.Release of the lactoferrin from the specific granules of PMN was enhanced by LT in vitro. Anti-55- but not anti-75-kDa TNF-R antibody enhanced the laccoferrin release. These antibodies failed to co-stimulate these PMN functions. The peak adhesiveness of PMN to a plastic plate and the peak expression of Mac-1 adhesion molecule (CD11b/CD18) on PMN were upregulated by LT in vitro. Anti-55- but not anti-75-kDa TNF-R antibody upregulated the peak adhesiveness of PMN and CD11b/CD18 expression mimicking LT.Though anti-75-kDa TNF-R antibody by itself did not alter the adhesiveness and marginally suppressed Mac-1 expression of PMN,it maintained the adhesiveness and adhesion molecule expression in the presence of anti-55-kDa TNF-R antibody. In summary, PMN predominantly express 75-kDa TNF-R,the signaling of LT (and TNF) in PMN is mediated mainly by 55-kDa TNF-R,and the adhesion function can be modulated also by 75-kDa TNF-R when 55-kDa TNF-R is stimulated.

用兔抗肿瘤坏死因子受体（TNF-R）多克隆抗体研究了体外培养的人中性粒细胞（PMN）55和75 kDa TNF-R的表达及其生物学作用。根据流式细胞术分析和γ I-LT结合试验，PMN主要表达75-kDa TNF-R<125>。在体外，PMN在人重组光敏素（LT）刺激下产生并释放超氧阴离子。抗-55-而不是抗-75-kDa TNF-R抗体刺激超氧化物释放模仿LT。释放的弹性蛋白酶从嗜天青颗粒的PMN在体外增强LT。抗-55-但不是抗-75-kDa TNF-R抗体增强了模拟LT的断裂酶释放。在体外，LT增强了从PMN特定颗粒释放乳铁蛋白。抗-55-但不是抗-75-kDa的TNF-R抗体增强了乳铁蛋白的释放。这些抗体未能共同刺激这些PMN功能。LT可上调PMN粘附分子Mac-1（CD 11b/CD 18）的表达。抗55 kDa TNF-R抗体可上调PMN的最大粘附率和CD 11b/CD 18的表达，但抗75 kDa TNF-R抗体本身并不改变PMN的最大粘附率，并略微抑制其Mac-1的表达，但在抗55 kDa TNF-R抗体存在下，可维持PMN的粘附分子和粘附分子的表达。总之，PMN主要表达75-kDa TNF-R，PMN中LT（和TNF）的信号传导主要由55-kDa TNF-R介导，并且当55-kDa TNF-R被刺激时，粘附功能也可由75-kDa TNF-R调节。

项目成果

Y Abe, Y Kashu et al.: "Idatification and biochemical characterization of human plasna neutrophil inhibitor in vitro." Surgery. 25. 139-144 (1995)

Y Abe、Y Kashu 等人：“人血浆中性粒细胞抑制剂的体外鉴定和生化特征。”

Y Abe, Y Osuka et al.: "The funtional role of 55- and 75-kDa tumor recrosis factor receptors in human polymorphonuclear cells in vitro." Cytokine. 7. 39-49 (1995)

Y Abe、Y Osuka 等人：“55-和 75-kDa 肿瘤坏死因子受体在体外人多形核细胞中的功能作用。”

Yashuhito Abe et al: "The functional role of 55-and 75-kDa tumor necrosis factor receptors in human polymophonuclear cells inv" Cytokine. (in press).

Yashuhito Abe 等人：“55-和 75-kDa 肿瘤坏死因子受体在人多形核细胞中的功能作用”细胞因子。

Y Abe,Y Kashu et al.: "Iden tification and biochemical choracterigation of human plasma neutrophil inhibitor in vitro." Surgery Today. 25. 139-144 (1995)

Y Abe，Y Kashu 等人：“人血浆中性粒细胞抑制剂的体外鉴定和生化鉴定”。

Yashuhito Abe et al.: "Plasma neutrophhil inhibitor(PNI):Identification and biochemical characterization" Surgery Today. (in press).

Yashuhito Abe 等人：“血浆中性粒细胞抑制剂（PNI）：鉴定和生化特征”《今日外科》。