DEFICIENCY OF IMMUNE INTERFERON-PRODUCTION BY LEUKOCYTES OF NORMAL NEWBORNS
DEFICIENCY OF IMMUNE INTERFERON-PRODUCTION BY LEUKOCYTES OF NORMAL NEWBORNS
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DOI：
10.1016/0008-8749(80)90150-1
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发表时间：
1980-01-01
影响因子：
4.3
通讯作者：
STIEHM, ER
中科院分区：
文献类型：
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作者：
BRYSON, YJ;WINTER, HS;STIEHM, ER
通过测量脐带血（N = 19）、1-7天龄新生儿（N = 19）和成人对照（N = 18）中分离的单核细胞的增殖反应和干扰素产生来评估[人]新生儿免疫系统的成熟度。在培养3-7天后，用植物血凝素（PHA）、混合白细胞培养物（MLC）中的同种异体白细胞或用胸苷脉冲的纽卡斯尔病病毒（NDV）刺激Ficoll-Hypaque分离的单核细胞，并测量胸苷掺入DNA并用于计算增殖指数。在最佳时间收获上清液用于测定经典和免疫干扰素（IF）的产生。在脑心肌炎病毒攻击后，使用人二倍体细胞通过微量滴定法评估IF。脐带和新生儿细胞的增殖反应相当于或大于成人对照。PHA诱导的免疫IF仅在19个脐带血中的1个和19个新生儿中的3个中产生; 2个单位）。新生儿MLC中无IF产生（373 . ±. 2 IU）、脐带（457 . ±. 2 IU）和成体细胞（170 . 3IU）。未通过T细胞数量或增殖反应检测到的新生儿细胞免疫异常被指示，并且与T细胞介导的细胞毒性（另一种专门的T细胞功能）中的类似缺陷平行。一个可能的机制，病毒感染的新生儿伴随细菌感染，并在患者进行移植物抗宿主反应，建议。
The maturity of the [human] newborn''s immune system was assessed by measuring proliferative responses and interferon production of isolated mononuclear cells from cord blood (N = 19), newborns 1-7 days of age (N = 19) and adult controls (N = 18). Ficoll-Hypaque-separated mononuclear cells were stimulated with phytohemagglutinin (PHA), allogeneic leukocytes in a mixed leukocyte culture (MLC) or Newcastle disease virus (NDV) pulsed with thymidine after 3-7 days in culture, and thymidine incorporation into DNA measured and used to calculate a proliferative index. The supernatants were harvested at optimal times for assay of classical and immune interferon (IF) production. IF was assessed by a microtiter assay using human diploid cells after encephalomyocarditis virus challenge. The proliferative responses of cord and newborn cells were equivalent or greater than those of adult controls. PHA-induced immune IF was produced in only 1 of 19 cord bloods and 3 of 19 newborns; immune IF was produced in all adults (225 .+-. 2 units). No IF was produced in MLC in newborn (373 .+-. 2IU), cord (457 .+-. 2IU) and adult cells (170 .+-. 3IU). An abnormality of cellular immunity in newborns, not detected by T cell numbers or proliferative responses, is indicated and parallels similar defects in T cell-mediated cytotoxicity, another specialized T cell function. A possible mechanism for viral infection in newborns with concomitant bacterial infections, and in patients undergoing graft vs. host reaction, is suggested.