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急性轮状病毒感染与循环记忆 CD4 T 细胞亚群的诱导有关。

Acute rotavirus infection is associated with the induction of circulating memory CD4 T cell subsets.

机构信息

Biological Sciences Departments, Malawi University of Science and Technology, Thyolo, Malawi.

Malawi Liverpool Wellcome Research Programme (MLW), Blantyre, Malawi.

出版信息

Sci Rep. 2023 Jun 2;13(1):9001. doi: 10.1038/s41598-023-35681-9.

DOI:10.1038/s41598-023-35681-9
PMID:37268634
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10238530/
Abstract

Strong CD4 T cell-mediated immune protection following rotavirus infection has been observed in animal models, but its relevance in humans remains unclear. Here, we characterized acute and convalescent CD4 T cell responses in children who were hospitalized with rotavirus-positive and rotavirus-negative diarrhoea in Blantyre, Malawi. Children presenting with laboratory-confirmed rotavirus infection had higher proportions of effector and central memory T helper 2 cells during acute infection i.e., at disease presentation compared to convalescence, 28 days post-infection defined by a follow-up 28 days after acute infection. However, circulating cytokine-producing (IFN-γ and/or TNF-α) rotavirus-specific VP6-specific CD4 T cells were rarely detectable in children with rotavirus infection at both acute and convalescent stages. Moreover, following whole blood mitogenic stimulation, the responding CD4 T cells were predominantly non-cytokine producers of IFN-γ and/or TNF-α. Our findings demonstrate limited induction of anti-viral IFN-γ and/or TNF-α-producing CD4 T cells in rotavirus-vaccinated Malawian children following the development of laboratory-confirmed rotavirus infection.

摘要

在动物模型中观察到轮状病毒感染后强烈的 CD4 T 细胞介导的免疫保护,但在人类中的相关性尚不清楚。在这里,我们对马拉维布兰太尔因轮状病毒阳性和轮状病毒阴性腹泻住院的儿童进行了急性和恢复期 CD4 T 细胞反应的特征分析。与恢复期相比,即急性感染时疾病表现时,在实验室确认轮状病毒感染的儿童中,效应和中央记忆 T 辅助 2 细胞的比例更高,感染后 28 天通过急性感染后 28 天的随访来定义。然而,在急性和恢复期,轮状病毒感染的儿童中很少能检测到循环细胞因子产生(IFN-γ 和/或 TNF-α)的轮状病毒特异性 VP6 特异性 CD4 T 细胞。此外,在全血有丝分裂刺激后,反应性 CD4 T 细胞主要是非 IFN-γ 和/或 TNF-α 细胞因子产生者。我们的研究结果表明,在马拉维接种轮状病毒的儿童中,实验室确认的轮状病毒感染后,针对病毒的 IFN-γ 和/或 TNF-α 产生 CD4 T 细胞的诱导有限。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/2c3534f90279/41598_2023_35681_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/e4a9800306f2/41598_2023_35681_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/7de7d11b575d/41598_2023_35681_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/2e83c19f35f3/41598_2023_35681_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/2c3534f90279/41598_2023_35681_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/e4a9800306f2/41598_2023_35681_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/7de7d11b575d/41598_2023_35681_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/2e83c19f35f3/41598_2023_35681_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b76/10238530/2c3534f90279/41598_2023_35681_Fig4_HTML.jpg

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