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首页> 外文期刊>Infection and immunity >Effects of gamma interferon, tumor necrosis factor alpha, and interleukin-2 on infection and proliferation of Theileria parva-infected bovine lymphoblasts and production of interferon by parasitized cells.
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Effects of gamma interferon, tumor necrosis factor alpha, and interleukin-2 on infection and proliferation of Theileria parva-infected bovine lymphoblasts and production of interferon by parasitized cells.

机译：γ干扰素，肿瘤坏死因子α和白细胞介素2对被Theileria parva感染的牛淋巴母细胞感染和增殖以及被寄生虫细胞产生干扰素的影响。

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Theileria parva is a protozoan parasite that infects bovine B cells and alpha beta and gamma delta T cells and transforms them into continually proliferating cells. CD4+ T. parva-antigen-specific immune T cells have been shown to produce cytokines in response to stimulation with parasitized cells, and T. parva-infected lymphocytes produce and consume T-cell growth factors and interleukin-2 (IL-2). To ascertain the role of T-cell cytokines on T. parva infections, we evaluated recombinant gamma interferon (rIFN-gamma), rIL-2, and tumor necrosis factor alpha (rTNF-alpha) for their effects on establishment, proliferation, and survival of parasitized cells. The results indicate that neither rIFN-gamma nor rTNF-alpha had an enhancing or inhibitory effect on the growth of established T. parva-infected T-cell clones, whereas bovine rIL-2 increased the proliferation of infected B-cell and alpha beta T-cell clones but not that of gamma delta T-cell clones. To evaluate the effects of the cytokines on establishment of parasitized cell lines, peripheral blood mononuclear cells were cultured in their presence immediately following infection with T. parva sporozoites. Neither rIFN-gamma nor rIL-2 altered the proportion of cells initially developing schizonts, but both enhanced establishment of infected cell lines by about twofold. In contrast, rTNF-alpha resulted in about a 33% decrease in the proportion of schizont-infected cells. Inhibitory effects on establishment of parasitized cell lines by rTNF-alpha were no longer apparent by 12 days following infection. Tests conducted during this study indicated that T. parva-infected lymphocytes also spontaneously produce IFN that is neutralized by acidic pH treatment. In conclusion, we speculate that none of these T-cell cytokines are likely to have a profound inhibitory effect in vivo on T. parva infections. Instead, IFN-gamma and IL-2 may facilitate the establishment of infection by T. parva.
机译：泰勒虫幼虫是一种原生动物寄生虫，可感染牛B细胞，αβ和γδT细胞并将其转化为持续增殖的细胞。已经显示，CD4 +帕瓦氏梭菌抗原特异性免疫T细胞会响应寄生虫细胞的刺激而产生细胞因子，感染帕氏梭菌的淋巴细胞会产生并消耗T细胞生长因子和白介素2（IL-2）。为了确定T细胞细胞因子在T. parva感染中的作用，我们评估了重组伽马干扰素（rIFN-γ），rIL-2和肿瘤坏死因子α（rTNF-alpha）对建立，增殖和存活的影响寄生细胞。结果表明，rIFN-γ和rTNF-α均未对已建立的经T. parva感染的T细胞克隆的生长产生增强或抑制作用，而牛rIL-2会增加受感染的B细胞和αβT的增殖。 -细胞克隆，但不包括γ-T细胞克隆。为了评估细胞因子对寄生虫细胞系建立的影响，在感染了帕尔沃螺旋体子孢子后立即在其存在下培养外周血单核细胞。 rIFN-γ和rIL-2都没有改变最初形成裂殖体的细胞比例，但是都将感染细胞系的建立提高了约两倍。相反，rTNF-α导致裂殖体感染细胞的比例下降了约33％。感染后12天，rTNF-α对寄生虫细胞系建立的抑制作用不再明显。在这项研究过程中进行的测试表明，感染了T. parva的淋巴细胞还自发产生了被酸性pH处理中和的IFN。总之，我们推测这些T细胞细胞因子均不可能在体内对T. parva感染产生深远的抑制作用。取而代之的是，IFN-γ和IL-2可能有助于建立帕氏梭菌感染。

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