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小鼠对微小隐孢子虫感染的免疫是通过肠道CD4 +上皮内淋巴细胞来表达的。

Immunity to Cryptosporidium muris infection in mice is expressed through gut CD4+ intraepithelial lymphocytes.

作者信息

McDonald V, Robinson H A, Kelly J P, Bancroft G J

机构信息

Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, London, United Kingdom.

出版信息

Infect Immun. 1996 Jul;64(7):2556-62. doi: 10.1128/iai.64.7.2556-2562.1996.

DOI:10.1128/iai.64.7.2556-2562.1996
PMID:8698479
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC174110/
Abstract

The role of gut intraepithelial lymphocytes (IEL) in immunity to cryptosporidial infection was investigated with a murine infection model involving Cryptosporidium muris. Oocyst shedding was monitored in severe combined immunodeficiency (SCID) mice infected with C. muris following intravenous injection of mesenteric lymph node (MLN) cells or intestinal IEL from BALB/c donor mice which were naive or previously infected with C. muris. SCID mice receiving no lymphoid cells developed chronic infections and excreted large numbers of oocysts until the end of the experiment. SCID mice injected with IEL from immune animals, however, were able to overcome the infection, and furthermore, these animals produced fewer oocysts and recovered sooner than ones which received IEL or MLN cells from naive BALB/c donors. Similar levels of protection were obtained in SCID mice injected with either 2 X 10(6) IEL or MLN cells from immune donor mice. Depletion of CD4+ cells from immune IEL, however, abrogated the ability to transfer immunity to SCID mice, while depletion of CD8+ cells only marginally reduced the protective capacity of immune IEL. Finally, control SCID mice which received no lymphocytes had < or = 1% CD4+ cells in the IEL from the small intestine, whereas the IEL from SCID mice recovered from infection, as a result of injection with immune IEL, contained 15% CD4+ cells. Thus, the ability to control C. muris infection correlated with the presence of the protective CD4+ cells in the gut epithelium.

摘要

利用涉及微小隐孢子虫的小鼠感染模型,研究了肠道上皮内淋巴细胞(IEL)在抵抗隐孢子虫感染免疫中的作用。在静脉注射来自未感染或先前感染过微小隐孢子虫的BALB/c供体小鼠的肠系膜淋巴结(MLN)细胞或肠道IEL后,监测严重联合免疫缺陷(SCID)小鼠感染微小隐孢子虫后的卵囊排出情况。未接受淋巴细胞的SCID小鼠发生慢性感染,并排出大量卵囊直至实验结束。然而,注射来自免疫动物的IEL的SCID小鼠能够克服感染,此外,这些动物产生的卵囊较少,且比接受来自未感染BALB/c供体的IEL或MLN细胞的小鼠恢复得更快。给SCID小鼠注射来自免疫供体小鼠的2×10⁶个IEL或MLN细胞可获得相似水平的保护。然而,从免疫IEL中去除CD4⁺细胞消除了将免疫力转移给SCID小鼠的能力,而去除CD8⁺细胞仅略微降低了免疫IEL的保护能力。最后,未接受淋巴细胞的对照SCID小鼠小肠IEL中的CD4⁺细胞≤1%,而由于注射免疫IEL从感染中恢复的SCID小鼠的IEL含有15%的CD4⁺细胞。因此,控制微小隐孢子虫感染的能力与肠道上皮中保护性CD4⁺细胞的存在相关。

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Immunity to Cryptosporidium muris infection in mice is expressed through gut CD4+ intraepithelial lymphocytes.小鼠对微小隐孢子虫感染的免疫是通过肠道CD4 +上皮内淋巴细胞来表达的。
Infect Immun. 1996 Jul;64(7):2556-62. doi: 10.1128/iai.64.7.2556-2562.1996.
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本文引用的文献

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Rat intestinal epithelial cell line IEC-6 is activated by recombinant interferon-gamma to inhibit replication of the coccidian Toxoplasma gondii.
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Cytokine synthesis by intestinal intraepithelial lymphocytes. Both gamma/delta T cell receptor-positive and alpha/beta T cell receptor-positive T cells in the G1 phase of cell cycle produce IFN-gamma and IL-5.肠道上皮内淋巴细胞的细胞因子合成。处于细胞周期G1期的γ/δ T细胞受体阳性和α/β T细胞受体阳性T细胞均产生干扰素-γ和白细胞介素-5。
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Toxoplasma gondii oral infection induces specific cytotoxic CD8 alpha/beta+ Thy-1+ gut intraepithelial lymphocytes, lytic for parasite-infected enterocytes.弓形虫经口感染可诱导产生特异性细胞毒性CD8α/β⁺ Thy-1⁺肠道上皮内淋巴细胞,对感染寄生虫的肠上皮细胞具有杀伤作用。
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Cryptosporidium muris in adult mice: adoptive transfer of immunity and protective roles of CD4 versus CD8 cells.成年小鼠中的微小隐孢子虫:免疫的过继转移以及CD4细胞与CD8细胞的保护作用
Infect Immun. 1994 Jun;62(6):2289-94. doi: 10.1128/iai.62.6.2289-2294.1994.
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Effect of spleen cell populations on resolution of Cryptosporidium parvum infection in SCID mice.脾细胞群体对重症联合免疫缺陷(SCID)小鼠中小隐孢子虫感染消退的影响。
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Differences in intraepithelial lymphocyte T cell subsets isolated from murine small versus large intestine.从小鼠小肠与大肠分离的上皮内淋巴细胞T细胞亚群的差异。
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