当前位置: X-MOL 学术AIDS Res. Hum. Retrovir. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Contribution of Innate Lymphoid Cells in Supplementing Cytokines Produced by CD4+ T Cells During Acute and Chronic SIV Infection of the Colon
AIDS Research and Human Retroviruses ( IF 1.5 ) Pub Date : 2022-09-12 , DOI: 10.1089/aid.2022.0007
Natasha Ferguson 1 , Andrew Cogswell 1 , Edward Barker 1
Affiliation  

HIV/SIV (simian immunodeficiency virus) infection leads to a loss of CD4+ T helper (Th) cells in number and function that begins during the acute phase and persists through the chronic phase of infection. In particular, there is a drastic decrease of Th17 and Th22 cells in the HIV/SIV-infected gastrointestinal (GI) tract as a source of interleukin (IL)-17 and IL-22. These cytokines are vital in the immune response to extracellular pathogens and maintenance of the GI tract. However, innate lymphoid cells (ILCs) are a source of IL-17 and IL-22 during the early stages of an immune response in mucosal tissue and remain vital cytokine producers when the immune response is persistent. Here, we wanted to determine whether ILCs are a source of IL-17 and IL-22 in the SIV-infected colon and could compensate for the loss of Th17 and Th22 cells. As a control, we evaluated the frequency and number of ILCs expressing interferon-gamma (IFNγ) and tumor necrosis factor-alpha (TNFα). We determined the frequency and number of cytokine expressing ILC subsets and T cell subsets within leukocytes from the colons of uninfected as well as acute and chronic SIV-infected colons without in vitro mitogenic stimulation. In the present study, we find that: (1) the frequency of IL-22, IFNγ, and TNFα but not IL-17 producing ILCs is increased in the acutely infected colon and remains high during the chronically infected colon relative to cytokine expressing ILCs in the uninfected colon, (2) ILCs are a significant source of IL-22, IFNγ, and TNFα but not IL-17 when CD4+ T lymphocytes in the gut lose their capacity to secrete these cytokines during SIV infection, and (3) the changes in the cytokines expressed by ILCs relative to CD4+ T cells in the infected colon were not due to increases in the frequency or number of ILCs in relation to T lymphocytes found in the tissue.

中文翻译:

结肠急性和慢性 SIV 感染期间先天淋巴细胞在补充 CD4+ T 细胞产生的细胞因子中的作用

HIV/SIV(猿猴免疫缺陷病毒)感染会导致 CD4 + T 辅助 (Th) 细胞的数量和功能丧失,这种情况从感染的急性期开始并持续到慢性期。特别是,在 HIV/SIV 感染的胃肠道 (GI) 中,作为白细胞介素 (IL)-17 和 IL-22 来源的 Th17 和 Th22 细胞急剧减少。这些细胞因子对于细胞外病原体的免疫反应和胃肠道的维持至关重要。然而,先天淋巴细胞 (ILC) 是粘膜组织免疫反应早期阶段 IL-17 和 IL-22 的来源,并且在免疫反应持续时仍然是重要的细胞因子产生者。在这里,我们想要确定 ILC 是否是 SIV 感染结肠中 IL-17 和 IL-22 的来源,并且可以补偿 Th17 和 Th22 细胞的损失。作为对照,我们评估了表达干扰素-γ (IFNγ) 和肿瘤坏死因子-α (TNFα) 的 ILC 的频率和数量。我们确定了未感染以及急性和慢性 SIV 感染结肠的白细胞内表达细胞因子的 ILC 子集和 T 细胞子集的频率和数量,而没有体外有丝分裂刺激。在本研究中,我们发现:(1)相对于表达细胞因子的 ILC,IL-22、IFNγ 和 TNFα 的频率在急性感染的结肠中增加,但在慢性感染的结肠中保持较高水平,但产生 IL-17 的 ILC 的频率不增加在未感染的结肠中,(2) 当肠道中的CD4 + T 淋巴细胞在 SIV 感染期间失去分泌这些细胞因子的能力时,ILC 是 IL-22、IFNγ 和 TNFα 的重要来源,但不是 IL-17,并且(3)受感染结肠中ILC 相对于 CD4 + T 细胞表达的细胞因子的变化并不是由于组织中发现的 ILC 相对于 T 淋巴细胞的频率或数量增加。
更新日期:2022-09-14
down
wechat
bug