MONOCLONAL ANTITUMOR NECROSIS FACTOR ANTIBODY RENDERS NONOBESE DIABETIC MICE HYPERSENSITIVE TO IRRADIATION AND ENHANCES INSULITIS DEVELOPMENT
MONOCLONAL ANTITUMOR NECROSIS FACTOR ANTIBODY RENDERS NONOBESE DIABETIC MICE HYPERSENSITIVE TO IRRADIATION AND ENHANCES INSULITIS DEVELOPMENT
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DOI：
10.1093/intimm/4.5.611
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发表时间：
1992-05-01
影响因子：
4.4
通讯作者：
MCDEVITT, HO
中科院分区：
文献类型：
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作者：
JACOB, CO;AISO, S;MCDEVITT, HO
为了评价肿瘤坏死因子的生物学作用，我们研究了抗肿瘤坏死因子单抗在非肥胖糖尿病(NOD)小鼠体内的作用。抗小鼠肿瘤坏死因子单抗使NOD小鼠对辐射致死效应过敏，并阻止过继转移淋巴细胞的致死照射小鼠的重建。在过继移植系统中，即使在移植后6天给予肿瘤坏死因子-α，也能降低糖尿病的发生率，但与对照小鼠相比，抗肿瘤坏死因子的单抗不能减少或增加糖尿病的发生率。给予肿瘤坏死因子-α4周或8周可显著降低NOD小鼠自发性胰岛素炎的发生率，而给予抗肿瘤坏死因子单抗8周可显著增加自发性胰岛素炎的发生率。
In attempt to evaluate biological roles of tumor necrosis factor (TNF), we studied the effects of anti-TNF mAb in non-obese diabetic (NOD) mice. Anti-murine TNF mAb rendered NOD mice hypersensitive to the lethal effects of radiation and prevented the reconstitution of lethally irradiated mice with adoptively transferred lymphocytes. While TNF-alpha reduced the incidence of diabetes development in the adoptive transfer system even when given 6 days post-transfer, mAb to TNF could not reduce or increase the incidence of diabetes compared to control mice. Administration of TNF-alpha for 4 or 8 weeks significantly reduced the incidence of spontaneous insulitis in NOD mice, while anti-TNF mAb given for 8 weeks increased the incidence of insulitis significantly.