Endogenous <scp>TWEAK</scp> is critical for regulating the function of mouse uterine natural killer cells in an immunological model of pregnancy loss

Qi, Xuefeng; Liu, Ming; Qin, Lijuan; Xie, Mengjie; Zhao, Dandan; Wang, Jingyu

doi:10.1111/imm.12588

Cited by 19 publications

(23 citation statements)

References 35 publications

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“…In particular, LPS stimulation induced the expression of Fn14 has been previously reported in vitro studies (Chacón et al, 2006; Qi et al, 2016). Similar results were observed in this study, we found that LPS-stimulated piglet have upregulated expression of TLR4 and Fn14 as well as decreased TWEAK expression in small intestine tissue compared to age matched untreated control piglets.…”

Section: Discussionmentioning

confidence: 65%

Lipopolysaccharide Upregulated Intestinal Epithelial Cell Expression of Fn14 and Activation of Fn14 Signaling Amplify Intestinal TLR4-Mediated Inflammation

Qin

et al. 2017

Front. Cell. Infect. Microbiol.

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TLR4 in intestinal epithelial cells has been shown both inflammatory and homeostatic roles following binding of its cognate ligand lipopolysaccharide (LPS). TWEAK-Fn14 axis plays an important role in pathologies caused by excessive or abnormal inflammatory responses. This study aimed to evaluate potential cross-talk between TLR4 and TWEAK/Fn14 system in porcine small intestinal epithelial cells. Our in vivo results showed that, compared with the age-matched normal control piglets, increased expression of Fn14 in epithelium and decreased TWEAK expression in lamina propria were detected in the small intestinal of piglets stimulated with LPS. Consistent with this finding, treatment with LPS increased the expression of Fn14 and TLR4 while decreased TWEAK expression in porcine small intestinal epithelial cell lines SIEC02. Interestingly, modulating Fn14 activation using agonistic anti-Fn14 decreased TLR4-mediated TNF-α production by SIEC02. In addition, pretreatment of LPS-stimulated SIEC02 with recombinant TWEAK protein suppresses the expression of Fn14 and TNF-α and inhibits the negative impact of LPS on the tight junctional protein occludin expression. In conclusion, this study demonstrates that the TWEAK-independent Fn14 activation augments TLR4-mediated inflammatory responses in the intestine of piglets. Furthermore, the TWEAK-dependent suppression of Fn14 signaling may play a role in intestinal homeostasis.

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Section: Discussionmentioning

confidence: 65%

Lipopolysaccharide Upregulated Intestinal Epithelial Cell Expression of Fn14 and Activation of Fn14 Signaling Amplify Intestinal TLR4-Mediated Inflammation

Qin

et al. 2017

Front. Cell. Infect. Microbiol.

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“…Furthermore, NK cell impairment to suppress the expansion and activity of Th17 cells, is identified in patients with recurrent spontaneous abortion [129]. Using the lipopolysaccharide-induced mouse abortion model, researchers found that in the uterus, a reduction of a tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in dNK cells and the upregulation of its receptor, may alter the cytotoxicity of dNK cells and, ultimately, result in pregnancy loss [158]. Quite recently, over-activated dNK cells, with an increased expression of angiogenic cytokines, such as VEGF-A and basic fibroblast growth factor, were observed in women with recurrent miscarriage, which suggests the potential relationship between the dysfunction of dNK cells in regulating angiogenesis and recurrent miscarriage [159].…”

Section: Reproductive Failurementioning

confidence: 99%

Innate Lymphoid Cells at the Maternal-Fetal Interface in Human Pregnancy

Chang¹,

Zhou²,

Li³

et al. 2020

Int. J. Biol. Sci.

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Pregnancy constitutes a major challenge to the maternal immune system, which must tolerate fetal alloantigen encoded by paternal genes. In addition to their role in inducing maternal-fetal immune tolerance, accumulating evidence indicates that decidual immune cells are involved in several processes required for a successful pregnancy, including trophoblast invasion as well as tissue and spiral artery remodeling. Innate lymphoid cells (ILCs), an important branch of the innate immune system, which has expanded rapidly in recent years, are strong actors in mucosal immunity, tissue homeostasis and metabolism regulation. With the recent identification of ILCs in the human decidua, the role of ILCs at the maternal-fetal interface raises concern. Herein, we review the presence and characterization of ILCs in the human decidua, as well as their function in normal pregnancy and pathological pregnancy, including reproductive failure, preeclampsia and others.

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“…Protein homogenates from goat cells were extracted as previously described (36). Briefly, the cells were lysed for 20 min on ice in ice-cold lysis buffer (Roche).…”

Section: Western Blot Analysismentioning

confidence: 99%

MicroRNA-1 Negatively Regulates Peripheral NK Cell Function via Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) Signaling Pathways During PPRV Infection

et al. 2020

Front. Immunol.

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Peste des petits ruminants virus (PPRV) has emerged as a significant threat to the productivity of small ruminants worldwide. PPRV is lymphotropic in nature and induces in the hosts a transient but severe immunosuppression, especially innate immunity. However, it remains largely unknown how NK cells respond and are regulated at the earliest time points after an acute viral PPRV infection in goats. In this study, we revealed that multiple immune responses of goat peripheral NK cells were compromised during PPRV infection, including the cytolytic effector molecule expression and cytokine production. Importantly, we demonstrated that PPRV infection stimulated the expression of TWEAK, a negative regulator of cytotoxic function of NK cells, which may be involved in the suppression of cytotoxicity as well as cytokine production in infected goat NK cells. Furthermore, we found that PPRV infection induced TWEAK expression in goat NK cells involving post-transcription by suppressing miR-1, a novel negative miRNA directly targeting the TWEAK gene. Moreover, replication of virus is required for inhibition of miR-1 expression during PPRV infection, and the non-structural V protein of PPRV plays an important role in miR-1 mediated TWEAK upregulation. Additionally, we revealed that the regulation of NK cell immune responses by TWEAK is mediated by MyD88, SOCS1, and STAT3. Taken together, our results demonstrated that TWEAK may play a key role in regulating goat peripheral NK cell cytotoxicity and cytokine expression levels during PPRV infection.

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Endogenous TWEAK is critical for regulating the function of mouse uterine natural killer cells in an immunological model of pregnancy loss

Cited by 19 publications

References 35 publications

Lipopolysaccharide Upregulated Intestinal Epithelial Cell Expression of Fn14 and Activation of Fn14 Signaling Amplify Intestinal TLR4-Mediated Inflammation

Lipopolysaccharide Upregulated Intestinal Epithelial Cell Expression of Fn14 and Activation of Fn14 Signaling Amplify Intestinal TLR4-Mediated Inflammation

Innate Lymphoid Cells at the Maternal-Fetal Interface in Human Pregnancy

MicroRNA-1 Negatively Regulates Peripheral NK Cell Function via Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) Signaling Pathways During PPRV Infection

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