Galectin-9 ameliorates respiratory syncytial virus-induced pulmonary immunopathology through regulating the balance between Th17 and regulatory T cells

Lu, Xin-Jiang; McCoy, Karen; Xu, Jianxiang; Hu, Wei; Chen, Hebin; Jiang, Kun; Feng, Hui; Chen, Peng; Wang, Yanli

doi:10.1016/j.virusres.2014.10.011

Cited by 25 publications

(21 citation statements)

References 38 publications

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“…Meanwhile, the percentage of Th17 cells and the concentration of IL-17 were significantly higher, compared to children suffering from a non-RSV pneumonia and healthy controls. When Galectin-9, an indirect inhibitor of Th1 and Th17 responses, was administered to RSV-infected mice, the viral load decreased, mucus production was inhibited and lung pathology diminished: these effects were achieved by inhibition of the Th17 response and induction of the Treg response (92). These studies show that an imbalance between Treg cells and Th17 cells might be an important pathogenic factor determining clinical severity of an RSV infection.…”

Section: Th17/treg Balance In Rsv and Its Clinical Relevancementioning

confidence: 79%

The role of Th17 and Treg responses in the pathogenesis of RSV infection

et al. 2015

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Section: Th17/treg Balance In Rsv and Its Clinical Relevancementioning

confidence: 79%

The role of Th17 and Treg responses in the pathogenesis of RSV infection

et al. 2015

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“…In parallel, an elevated level of Th17 cells was found pathogenic in RSV infection, leading to enhanced mucus production and neutrophile infiltration. As a result, this imbalance of Treg and Th17 cells in RSV infection could cause damage to the lung, and it was demonstrated that RSV‐induced pulmonary immunopathology could be ameliorated by inhibiting Th17 cell production and boosting Treg expansion . Therefore, the imbalance of Treg and Th17 cells may be an important causative factor in determining the clinical severity of RSV infection.…”

Section: Treg and Th17 Cells In Rsv Infectionmentioning

confidence: 99%

Regulatory T cells and T helper 17 cells in viral infection

et al. 2020

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CD4 + T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 + T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection. How to cite this article: Wan Z, Zhou Z, Liu Y, et al. Regulatory T cells and T helper 17 cells in viral infection. Scand J Immunol. 2020;91:e12873.

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“…Gal-9 is identified as a Tim-3 ligand and the Gal-9/Tim-3 interaction acts as a specific inhibitor of T helper (Th)1 and Th17 immune responses13; however studies have shown that Gal-9 also binds to CD4414, CD13715, and protein disulfide isomerase (PDI)16. In addition, high-mobility group box 1 (HMGB-1) also binds to Tim-317.…”

mentioning

confidence: 99%

Blockage of Galectin-receptor Interactions by α-lactose Exacerbates Plasmodium berghei-induced Pulmonary Immunopathology

Liu

Huang

et al. 2016

Sci Rep

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Malaria-associated acute lung injury (ALI) is a frequent complication of severe malaria that is often caused by “excessive” immune responses. To better understand the mechanism of ALI in malaria infection, here we investigated the roles of galectin (Gal)-1, 3, 8, 9 and the receptors of Gal-9 (Tim-3, CD44, CD137, and PDI) in malaria-induced ALI. We injected alpha (α)-lactose into mice-infected with Plasmodium berghei ANKA (PbANKA) to block galectins and found significantly elevated total proteins in bronchoalveolar lavage fluid, higher parasitemia and tissue parasite burden, and increased numbers of CD68+ alveolar macrophages as well as apoptotic cells in the lungs after blockage. Additionally, mRNA levels of Gal-9, Tim-3, CD44, CD137, and PDI were significantly increased in the lungs at day 5 after infection, and the levels of CD137, IFN-α, IFN-β, IFN-γ, IL-4, and IL-10 in the lungs were also increased after α-lactose treatment. Similarly, the levels of Gal-9, Tim-3, IFN-α, IFN-β, IFN-γ, and IL-10 were all significantly increased in murine peritoneal macrophages co-cultured with PbANKA-infected red blood cells in vitro; but only IFN-α and IFN-β were significantly increased after α-lactose treatment. Our data indicate that Gal-9 interaction with its multiple receptors play an important role in murine malaria-associated ALI.

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Galectin-9 ameliorates respiratory syncytial virus-induced pulmonary immunopathology through regulating the balance between Th17 and regulatory T cells

Cited by 25 publications

References 38 publications

The role of Th17 and Treg responses in the pathogenesis of RSV infection

The role of Th17 and Treg responses in the pathogenesis of RSV infection

Regulatory T cells and T helper 17 cells in viral infection

Blockage of Galectin-receptor Interactions by α-lactose Exacerbates Plasmodium berghei-induced Pulmonary Immunopathology

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