Wiedermann U, Hanson L A, Kahu H, Dahlgren U I
Department of Clinical Immunology, University of Göteborg, Sweden.
Immunology. 1993 Dec;80(4):581-6.
We have previously reported that vitamin A deficiency resulted in a reduced IgA antibody response to cholera toxin (CT) after per-oral immunization. In the present investigation we have studied the in vivo and in vitro immune response in vitamin A-deficient rats to two parenterally applied antigens, beta-lactoglobulin (beta-LG) and picrylsulphonic acid (TNP)-Ficoll. The serum IgG and IgM antibody responses to the T-cell dependent antigen beta-LG were significantly lower in the vitamin A-deficient rats than in the pair-fed control rats. No such differences were seen with the IgG and IgM responses to the T-cell independent antigen TNP-Ficoll. However, the biliary IgA and the serum IgE antibodies against both antigens were decreased in the vitamin A-deficient rats. In vitro lymphocyte stimulation with concanavalin A (Con A) or beta-LG gave higher T-cell proliferation rates in the vitamin A-deficient than in the control rats. Interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) levels in supernatants from Con A-stimulated mesenteric lymph node cells were also higher in the vitamin A-deficient rats, while IL-6 levels were decreased, which is consistent with an up-regulated Th1 activity. Proliferation studies on purified accessory cells and T cells from the deficient and the control rats, mixed in different combinations, showed that the T cells, but not the accessory cells, were disturbed in the vitamin A-deficient rats. Despite the increased T-cell activity in vitro the vitamin A-deficient rats had a lower delayed-type hypersensitivity (DTH) reaction than the pair-fed control rats. In conclusion, the increased IL-2 and IFN-gamma levels may reflect an up-regulation of Th1 cell function, while the decreased IgA, IgE and IL-6 levels indicate a suppression of Th2 cells. The disturbed T-lymphocyte function is manifested in vivo as a decreased DTH reaction and suppressed antibody production, the latter possibly due to a lack of B-cell switching and proliferation factors in vitamin A-deficient rats.
我们之前曾报道，维生素A缺乏会导致经口免疫后对霍乱毒素（CT）的IgA抗体反应降低。在本研究中，我们研究了维生素A缺乏大鼠对两种经肠胃外施用的抗原，即β-乳球蛋白（β-LG）和苦味酸磺酸（TNP）-菲可的体内和体外免疫反应。维生素A缺乏大鼠对T细胞依赖性抗原β-LG的血清IgG和IgM抗体反应明显低于配对喂养的对照大鼠。对T细胞非依赖性抗原TNP-菲可的IgG和IgM反应未观察到此类差异。然而，维生素A缺乏大鼠中针对这两种抗原的胆汁IgA和血清IgE抗体减少。用刀豆蛋白A（Con A）或β-LG进行体外淋巴细胞刺激时，维生素A缺乏大鼠的T细胞增殖率高于对照大鼠。Con A刺激的肠系膜淋巴结细胞上清液中的白细胞介素-2（IL-2）和干扰素-γ（IFN-γ）水平在维生素A缺乏大鼠中也较高，而IL-6水平降低，这与Th1活性上调一致。对来自缺乏和对照大鼠的纯化辅助细胞和T细胞以不同组合混合进行的增殖研究表明，维生素A缺乏大鼠中的T细胞而非辅助细胞受到干扰。尽管体外T细胞活性增加，但维生素A缺乏大鼠的迟发型超敏反应（DTH）比配对喂养的对照大鼠低。总之，IL-2和IFN-γ水平升高可能反映了Th1细胞功能的上调，而IgA、IgE和IL-6水平降低表明Th2细胞受到抑制。T淋巴细胞功能紊乱在体内表现为DTH反应降低和抗体产生受到抑制，后者可能是由于维生素A缺乏大鼠中缺乏B细胞转换和增殖因子。
