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CD8+ T cells with high TGF??1 expression cause lymph node fibrosis following HIV infection.

ABSTRACT: Lymph node (LN) fibrosis resulting in cluster of differentiation (CD) 4+ T cell reduction following human immunodeficiency virus (HIV) infection is an important step in the pathogenesis of acquired immunodeficiency syndrome. The mechanisms mediating LN fibrosis following HIV infection have not been completely elucidated. In order to investigate the mechanism of LN fibrosis, the expression of transforming growth factor (TGF)??1 was determined in the LNs of HIV?infected individuals by immunohistochemistry and fluorescence?based flow cytometry. The effect of stimulated CD8+ T cells on collagen secretion by fibroblasts was detected using immunofluorescence staining and western blot analysis. The results demonstrated that the LNs of HIV?infected individuals exhibited a significantly increased proportion of CD8+ T cells with high TGF??1 expression. These CD8+ T cells demonstrated increased CD38 and programmed cell death protein 1 expression and decreased CD127 expression compared with the controls. CD8+ T cells from the LNs of non?HIV infected individuals expressed a high TGF??1 level following stimulation with phorbol?12?myristate 13?acetate. These CD8+T cells subsequently induced the secretion of a large amount of type I collagen in human lymphatic fibroblasts. The results of the present study indicated that CD8+ T cells with high TGF??1 expression served an important role in LN fibrosis following HIV infection.

SUBMITTER: Huang L

PROVIDER: S-EPMC6059705 | biostudies-other | 2018 Jul

REPOSITORIES: biostudies-other

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CD8+ T cells with high TGF‑β1 expression cause lymph node fibrosis following HIV infection.

Huang Lei L Deng Jianning J Xu Wen W Wang Hongbo H Shi Lei L Wu Fengyao F Wu Dan D Nei Weimin W Zhao Min M Mao Panyong P Zhou Xianzhi X

Molecular medicine reports 20180503 1

Lymph node (LN) fibrosis resulting in cluster of differentiation (CD) 4+ T cell reduction following human immunodeficiency virus (HIV) infection is an important step in the pathogenesis of acquired immunodeficiency syndrome. The mechanisms mediating LN fibrosis following HIV infection have not been completely elucidated. In order to investigate the mechanism of LN fibrosis, the expression of transforming growth factor (TGF)‑β1 was determined in the LNs of HIV‑infected individuals by immunohistoc ...[more]

PMID: 29749506

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Project description:Although the primary organ has been the subject of intense investigation in the field of organ fibrosis over the past several decades, the presence of lymph node fibrosis due to persistent activation of the immune response in its partner organ remains largely unknown. Previously, we demonstrated that activation of the immune response following ischemia-reperfusion injury (IRI) and crescentic glomerulonephritis (CGN) in the kidney was associated with extracellular matrix (ECM) production by fibroblastic reticular cells (FRCs) of the kidney-draining lymph node (KLN). Here, we sought to determine whether FRCs in the KLN become similarly fibrogenic following unilateral ureteral obstruction (UUO) of the kidney. We subjected 6-8-week-old C57BL/6J mice to UUO for 2, 7, and 14 days. We examined the microarchitecture of the kidney and KLN by immunofluorescence staining at each timepoint, and we quantified immune cell populations in the KLN by flow cytometry. The contralateral kidney unaffected by UUO and its partner KLN were used as controls. We found through immunofluorescence staining that FRCs increased production of ECM fibers and remodeled the microarchitecture of the UUO KLN, contributing to fibrosis that mirrored the changes in the kidney. We also observed by flow cytometry that the populations of CD11b+ antigen-presenting cells, CD11c+ dendritic cells, and activated CD4+ and CD8+ T cells were significantly higher in the UUO KLN than the KLN draining the unaffected contralateral kidney. Expression of the TGFβ/TGFβR signaling pathway was upregulated and colocalized with FRCs in the UUO KLNs, suggesting a possible mechanism behind the fibrosis. Both release of ureteral ligation at 2 days following UUO and depletion of FRCs at the time of injury onset halted the progression of fibrosis in both the kidney and the KLN. These findings for the first time highlight the association between fibrosis both in the kidney and the KLN during UUO, and they lay the groundwork for future studies that will investigate more deeply the mechanisms behind the connection between FRCs and KLN fibrosis.

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CD8+ T cells with high TGF??1 expression cause lymph node fibrosis following HIV infection.

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CD8+ T cells with high TGF‑β1 expression cause lymph node fibrosis following HIV infection.

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