tigit targeting lentiviruses Search Results


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Angel Biotechnology tigit targeting lentiviruses
<t>TIGIT</t> upregulation on NK cells impairs their antifibrotic function during schistosomiasis infection. (A) Representative HE and Masson staining of liver tissue from control (WT)and S. japonicum –infected (SJ) mice at 6 weeks post-infection showing egg deposition and collagen accumulation. (B) Quantification of granulomatous inflammatory cell infiltration. (C) Quantification of collagen fiber deposition. (D) Liver-to-body weight ratio in control and infected mice. (E) Relative hepatic mRNA expression levels of Acta2 , Col I , Fn , and Tigit at different time points post-infection. (F) Flow cytometric gating strategy for NK cells (CD3 − NK1.1 + ) from hepatic nonparenchymal cells. (G) Proportion of NK cells at 0, 4, 6, and 8 weeks post-infection. (H) Percentage of TIGIT + NK cells during infection. (I, J) Percentages of IFNγ + and GZMB + NK cells at different infection stages. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Tigit Targeting Lentiviruses, supplied by Angel Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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TIGIT upregulation on NK cells impairs their antifibrotic function during schistosomiasis infection. (A) Representative HE and Masson staining of liver tissue from control (WT)and S. japonicum –infected (SJ) mice at 6 weeks post-infection showing egg deposition and collagen accumulation. (B) Quantification of granulomatous inflammatory cell infiltration. (C) Quantification of collagen fiber deposition. (D) Liver-to-body weight ratio in control and infected mice. (E) Relative hepatic mRNA expression levels of Acta2 , Col I , Fn , and Tigit at different time points post-infection. (F) Flow cytometric gating strategy for NK cells (CD3 − NK1.1 + ) from hepatic nonparenchymal cells. (G) Proportion of NK cells at 0, 4, 6, and 8 weeks post-infection. (H) Percentage of TIGIT + NK cells during infection. (I, J) Percentages of IFNγ + and GZMB + NK cells at different infection stages. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Frontiers in Immunology

Article Title: TIGIT impairs NK cell antifibrotic activity through the IFNγ–IFI30 axis in schistosomiasis-induced liver fibrosis

doi: 10.3389/fimmu.2026.1766930

Figure Lengend Snippet: TIGIT upregulation on NK cells impairs their antifibrotic function during schistosomiasis infection. (A) Representative HE and Masson staining of liver tissue from control (WT)and S. japonicum –infected (SJ) mice at 6 weeks post-infection showing egg deposition and collagen accumulation. (B) Quantification of granulomatous inflammatory cell infiltration. (C) Quantification of collagen fiber deposition. (D) Liver-to-body weight ratio in control and infected mice. (E) Relative hepatic mRNA expression levels of Acta2 , Col I , Fn , and Tigit at different time points post-infection. (F) Flow cytometric gating strategy for NK cells (CD3 − NK1.1 + ) from hepatic nonparenchymal cells. (G) Proportion of NK cells at 0, 4, 6, and 8 weeks post-infection. (H) Percentage of TIGIT + NK cells during infection. (I, J) Percentages of IFNγ + and GZMB + NK cells at different infection stages. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The control and TIGIT -targeting lentiviruses were packaged and synthesized by Angel Biotechnology Co., Ltd. (Suzhou, China).

Techniques: Infection, Staining, Control, Expressing

TIGIT knockdown enhances IFNγ production and partially restores NK92 cell cytotoxicity. (A) GFP fluorescence confirming successful lentiviral transduction of TIGIT -knockdown (KD) NK92 cells. (B) RT-qPCR verification of TIGIT knockdown efficiency. (C, D) Representative flow cytometry plots of IFNγ and GZMB expression in control (NC) and TIGIT -KD (KD) NK92 cells. (E, F) Quantification of IFNγ + and GZMB + cell proportions. (G–I) Flow cytometric analysis of apoptosis in LX-2 cells after co-culture with NC or TIGIT -KD NK92 cells for 6 h, showing increased early and late apoptosis induced by TIGIT knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Frontiers in Immunology

Article Title: TIGIT impairs NK cell antifibrotic activity through the IFNγ–IFI30 axis in schistosomiasis-induced liver fibrosis

doi: 10.3389/fimmu.2026.1766930

Figure Lengend Snippet: TIGIT knockdown enhances IFNγ production and partially restores NK92 cell cytotoxicity. (A) GFP fluorescence confirming successful lentiviral transduction of TIGIT -knockdown (KD) NK92 cells. (B) RT-qPCR verification of TIGIT knockdown efficiency. (C, D) Representative flow cytometry plots of IFNγ and GZMB expression in control (NC) and TIGIT -KD (KD) NK92 cells. (E, F) Quantification of IFNγ + and GZMB + cell proportions. (G–I) Flow cytometric analysis of apoptosis in LX-2 cells after co-culture with NC or TIGIT -KD NK92 cells for 6 h, showing increased early and late apoptosis induced by TIGIT knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The control and TIGIT -targeting lentiviruses were packaged and synthesized by Angel Biotechnology Co., Ltd. (Suzhou, China).

Techniques: Knockdown, Fluorescence, Transduction, Quantitative RT-PCR, Flow Cytometry, Expressing, Control, Co-Culture Assay

TIGIT downregulation alters IFI30 expression and promotes NK cell activation. (A) Volcano plot of differentially expressed genes. (B) KEGG pathway enrichment analysis of upregulated genes showing enrichment in cytokine and apoptotic signaling pathways. (C–E) Validation of Ifi30 , Gzmb , and Ifnγ expression by RT-qPCR and WB, confirming IFI30 upregulation following Tigit knockdown. (F, G) Flow cytometric analysis of cell cycle distribution and quantification of S-phase proportion, indicating enhanced proliferation after Tigit knockdown. (H–J) RT-qPCR and WB analyses showing that IFNγ antagonist treatment downregulates Ifi30 and Bcl2 while increasing Bax expression, suggesting that the IFNγ–IFI30 axis regulates NK cell proliferation and apoptosis. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Frontiers in Immunology

Article Title: TIGIT impairs NK cell antifibrotic activity through the IFNγ–IFI30 axis in schistosomiasis-induced liver fibrosis

doi: 10.3389/fimmu.2026.1766930

Figure Lengend Snippet: TIGIT downregulation alters IFI30 expression and promotes NK cell activation. (A) Volcano plot of differentially expressed genes. (B) KEGG pathway enrichment analysis of upregulated genes showing enrichment in cytokine and apoptotic signaling pathways. (C–E) Validation of Ifi30 , Gzmb , and Ifnγ expression by RT-qPCR and WB, confirming IFI30 upregulation following Tigit knockdown. (F, G) Flow cytometric analysis of cell cycle distribution and quantification of S-phase proportion, indicating enhanced proliferation after Tigit knockdown. (H–J) RT-qPCR and WB analyses showing that IFNγ antagonist treatment downregulates Ifi30 and Bcl2 while increasing Bax expression, suggesting that the IFNγ–IFI30 axis regulates NK cell proliferation and apoptosis. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The control and TIGIT -targeting lentiviruses were packaged and synthesized by Angel Biotechnology Co., Ltd. (Suzhou, China).

Techniques: Expressing, Activation Assay, Protein-Protein interactions, Biomarker Discovery, Quantitative RT-PCR, Knockdown

NK cell–specific Tigit knockout alleviates schistosomiasis-induced liver fibrosis in vivo . (A) Representative HE and Masson staining of liver tissue from WT and Tigit -knockout mice 6 weeks post-infection. (B, C) Quantification of inflammatory infiltration and collagen deposition. (D) Liver-to-body weight ratio in WT and Tigit -knockout mice. (E) RT-qPCR analysis of Acta2 , Col1a1 , Fn , and Tigit mRNA expression in hepatic tissue. (F, G) WB detection and quantification of α-SMA, COL1, TIGIT, and IFI30 protein levels. (H, I) Flow cytometry and quantification showing increased NK cell proportions in Tigit -knockout mice. (J, K) Frequency of TIGIT + NK cells. (L, M) Proportions of IFNγ + and NK cells, demonstrating enhanced NK cell activation following Tigit knockout. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Frontiers in Immunology

Article Title: TIGIT impairs NK cell antifibrotic activity through the IFNγ–IFI30 axis in schistosomiasis-induced liver fibrosis

doi: 10.3389/fimmu.2026.1766930

Figure Lengend Snippet: NK cell–specific Tigit knockout alleviates schistosomiasis-induced liver fibrosis in vivo . (A) Representative HE and Masson staining of liver tissue from WT and Tigit -knockout mice 6 weeks post-infection. (B, C) Quantification of inflammatory infiltration and collagen deposition. (D) Liver-to-body weight ratio in WT and Tigit -knockout mice. (E) RT-qPCR analysis of Acta2 , Col1a1 , Fn , and Tigit mRNA expression in hepatic tissue. (F, G) WB detection and quantification of α-SMA, COL1, TIGIT, and IFI30 protein levels. (H, I) Flow cytometry and quantification showing increased NK cell proportions in Tigit -knockout mice. (J, K) Frequency of TIGIT + NK cells. (L, M) Proportions of IFNγ + and NK cells, demonstrating enhanced NK cell activation following Tigit knockout. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The control and TIGIT -targeting lentiviruses were packaged and synthesized by Angel Biotechnology Co., Ltd. (Suzhou, China).

Techniques: Knock-Out, In Vivo, Staining, Infection, Quantitative RT-PCR, Expressing, Flow Cytometry, Activation Assay

Proposed working model of the TIGIT–IFNγ–IFI30 signaling axis in schistosomiasis-induced liver fibrosis. Schematic illustration showing that upregulation of TIGIT on NK cells during S. japonicum infection suppresses IFNγ secretion and downregulates IFI30 expression, leading to NK cell exhaustion and reduced cytotoxicity toward hepatic stellate cells. Conversely, TIGIT knockout restores IFNγ–IFI30 signaling, promotes NK cell proliferation and function, and mitigates hepatic fibrosis progression.

Journal: Frontiers in Immunology

Article Title: TIGIT impairs NK cell antifibrotic activity through the IFNγ–IFI30 axis in schistosomiasis-induced liver fibrosis

doi: 10.3389/fimmu.2026.1766930

Figure Lengend Snippet: Proposed working model of the TIGIT–IFNγ–IFI30 signaling axis in schistosomiasis-induced liver fibrosis. Schematic illustration showing that upregulation of TIGIT on NK cells during S. japonicum infection suppresses IFNγ secretion and downregulates IFI30 expression, leading to NK cell exhaustion and reduced cytotoxicity toward hepatic stellate cells. Conversely, TIGIT knockout restores IFNγ–IFI30 signaling, promotes NK cell proliferation and function, and mitigates hepatic fibrosis progression.

Article Snippet: The control and TIGIT -targeting lentiviruses were packaged and synthesized by Angel Biotechnology Co., Ltd. (Suzhou, China).

Techniques: Infection, Expressing, Knock-Out