Koster F, Pierce N F
Clin Exp Immunol. 1985 Apr;60(1):217-24.
Secretory IgA antibody responses such as those directed against respiratory and enteric pathogens, may be impaired in protein-calorie malnutrition. In previous studies using a rat model of the mucosal immune response to cholera toxin, as little as 2 weeks of severe protein deprivation markedly impaired mucosal anti-toxin production. The present studies examined the effect of protein deprivation on lymphocyte populations which adoptively transfer either priming or suppression of a mucosal anti-toxin response from malnourished donor rats to syngeneic well nourished recipients. Either 2 or 8 weeks of protein deprivation severely impaired the development of thoracic duct lymphocytes which could transfer priming or suppression after intraduodenal priming, and impaired splenic suppressor cell development after s.c. priming. The abrogation of suppression by protein deprivation was dependent on the dose of s.c. antigen used to induce suppression. Refeeding rats after two months of protein deprivation led to recovery of both priming cell and suppressor cell function. Severe protein deprivation induces a reversible defect in both priming and suppressor cell populations; the net effect is an impaired mucosal immune response.
诸如针对呼吸道和肠道病原体的分泌型IgA抗体反应,在蛋白质 - 热量营养不良时可能会受损。在先前使用大鼠对霍乱毒素黏膜免疫反应模型的研究中,仅2周的严重蛋白质缺乏就显著损害了黏膜抗毒素的产生。本研究考察了蛋白质缺乏对淋巴细胞群体的影响,这些淋巴细胞群体可将营养不良供体大鼠的黏膜抗毒素反应的启动或抑制作用过继转移给同基因营养良好的受体。2周或8周的蛋白质缺乏严重损害了胸导管淋巴细胞的发育,这些淋巴细胞在十二指肠内启动后可转移启动或抑制作用,并且在皮下启动后损害了脾抑制细胞的发育。蛋白质缺乏对抑制作用的消除取决于用于诱导抑制的皮下抗原剂量。蛋白质缺乏两个月后再给大鼠喂食可导致启动细胞和抑制细胞功能的恢复。严重的蛋白质缺乏会在启动细胞和抑制细胞群体中诱导出可逆的缺陷;最终结果是黏膜免疫反应受损。