Ifn Signaling(Ifn 시그널링)란 무엇입니까?
Ifn Signaling Ifn 시그널링 - RESULTS SARS-CoV-2 copies, angiotensin-converting enzyme 2, and TMPRSS2 gene expression were similar in children and adults, but children displayed higher expression of genes associated with IFN signaling, NLRP3 inflammasome, and other innate pathways. [1] The present results indicate that tumor progression is regulated by CLCN2 through its effects on IFN signaling. [2] Treatment with exogenous IL-22 blocked rotavirus replication in microbiota-depleted wild-type and Stat1-/- mice, demonstrating that the antiviral effect of IL-22 in animals with altered microbiome is not dependent on IFN signaling. [3] IFN signaling had minor effects on PR8 replication and contributed to controlling neutrophilic inflammation and hemorrhagic lung pathology in RV/PR8-infected mice. [4] Interferon gamma (IFNγ) represents a major driving force behind PD-L1 expression in tumor microenvironment, and histone deacetylase 2 (HDAC2) is required for IFN signaling. [5] These genes were associated with cellular antigen processing and presentation and IFN signaling. [6] A rapidly growing body of work has interrogated the mechanisms by which SARS-CoV-2 antagonizes both IFN induction and IFN signaling to establish productive infection. [7] Here we show that TRAIL and the Smac mimetic LCL161 induce non-canonical NF-κB and IFN signaling in ER-positive MCF-7 cells and in CAMA-1 breast cancer cells when apoptosis is blocked by caspase inhibition. [8] Here, we used genome-wide loss-of-function screening to establish genes critical for IFN signaling, identifying all expected members of the JAK-STAT pathway and the previously unappreciated bromodomain-containing protein 9 (BRD9), a defining subunit of non-canonical BAF (ncBAF) chromatin remodeling complexes. [9] The main mechanisms of these components are MAPK signaling, PI3K signaling, TGFB signaling, JAK-STAT signaling, TLR signaling, RLR signaling, IFN Signaling, chemokine signaling, cell cycle, apoptosis, transcription. [10] In turn, viruses have evolved numerous countermeasures to avoid the effects of IFN signaling. [11] Impaired mucosal healing in double IFN receptor-deficient mice is driven by decreased amphiregulin expression, which IFN signaling can up-regulate in either the epithelial or hematopoietic compartment. [12] IFN signaling then requires IRF9 for the expression of the full array of interferon stimulated genes (ISGs) ultimately defining the antiviral state of the cell. [13]결과 SARS-CoV-2 사본, 안지오텐신 전환 효소 2 및 TMPRSS2 유전자 발현은 어린이와 성인에서 유사했지만 어린이는 IFN 신호 전달, NLRP3 인플라마솜 및 기타 선천적 경로와 관련된 유전자의 발현이 더 높았습니다. [1] 현재 결과는 종양 진행이 IFN 신호전달에 대한 효과를 통해 CLCN2에 의해 조절됨을 나타냅니다. [2] 외인성 IL-22 처리는 미생물군이 고갈된 야생형 및 Stat1-/- 마우스에서 로타바이러스 복제를 차단하여 미생물군집이 변경된 동물에서 IL-22의 항바이러스 효과가 IFN 신호전달에 의존하지 않음을 보여줍니다. [3] IFN 신호전달은 PR8 복제에 미미한 영향을 미쳤고 RV/PR8에 감염된 마우스에서 호중구 염증 및 출혈성 폐 병리를 조절하는 데 기여했습니다. [4] 인터페론 감마(IFNγ)는 종양 미세환경에서 PD-L1 발현의 주요 원동력이며 IFN 신호전달에는 히스톤 데아세틸라제 2(HDAC2)가 필요합니다. [5] 이들 유전자는 세포 항원 처리 및 제시 및 IFN 신호전달과 관련이 있었다. [6] 빠르게 성장하는 작업은 SARS-CoV-2가 IFN 유도 및 IFN 신호 전달을 모두 길항하여 생산적인 감염을 확립하는 메커니즘을 조사했습니다. [7] 여기에서 우리는 TRAIL 및 Smac 모방 LCL161이 카스파제 억제에 의해 세포자멸사가 차단될 때 ER-양성 MCF-7 세포 및 CAMA-1 유방암 세포에서 비표준 NF-κB 및 IFN 신호전달을 유도한다는 것을 보여줍니다. [8] 여기에서 우리는 IFN 신호 전달에 중요한 유전자를 설정하기 위해 게놈 전체의 기능 상실 스크리닝을 사용하여 JAK-STAT 경로의 모든 예상 구성원과 이전에 평가되지 않은 브로모도메인 함유 단백질 9(BRD9)를 식별했습니다. 표준 BAF(ncBAF) 염색질 리모델링 복합체. [9] 이러한 구성 요소의 주요 메커니즘은 MAPK 신호, PI3K 신호, TGFB 신호, JAK-STAT 신호, TLR 신호, RLR 신호, IFN 신호, 케모카인 신호, 세포 주기, 세포 사멸, 전사입니다. [10] 차례로, 바이러스는 IFN 신호 전달의 영향을 피하기 위해 수많은 대응책을 발전시켰습니다. [11] 이중 IFN 수용체 결핍 마우스에서 손상된 점막 치유는 암피레귤린 발현 감소에 의해 유발되며, 이는 IFN 신호가 상피 또는 조혈 구획에서 상향 조절될 수 있습니다. [12] IFN 신호 전달은 궁극적으로 세포의 항바이러스 상태를 정의하는 인터페론 자극 유전자(ISG)의 전체 어레이의 발현을 위해 IRF9를 필요로 합니다. [13]
I Ifn Signaling I Ifn 시그널링
Inhibition of type I IFN signaling increased PbT-II and partially reversed the Th1 over Tfh bias of the PbT-II cells in both PbA- and Pcc-infected mice. [1] A set of interferon simulated genes (ISGs) are then expressed in response to type I IFN signaling to set the cells in the antiviral state. [2] Here, we report that CCDC50, a newly identified autophagy receptor, tunes STING-directed type I IFN signaling activity by delivering K63-polyubiquitinated STING to autolysosomes for degradation. [3] 167–175) identify a potential key role for type I IFN signaling for DIC in human patients with septic shock and for endothelial cell (EC) injury, inflammation, andfibrinolysis (2). [4] Apoptotic caspases have recently emerged as important regulators of type I IFN signaling in both non-infectious contexts and during viral infection2–5. [5] When reimplanted into mice, resistant tumors were more sensitive to IL-6 inhibition (a key PTIS component) and growth significantly reduced when type I IFN signaling was blocked. [6] The mRNA and protein expressions of ISGs and type I IFN signaling pathway components were evaluated by quantitative real-time polymerase chain reaction, western blot, immunofluorescence, and/or immunohistochemistry. [7] These results collectively indicated that AjIκBα function as an important negative regulation in innate immunity of host against antibacterial and antiviral infection likely via the inhibition of the activation of NF-κB, AP1, and type I IFN signaling pathways. [8] find that type I IFN signaling contributes to the death of Mtb-infected macrophages through an apparently novel mechanism. [9] In conclusion, these findings indicate that hIFIT5 is a negative modulator in the type I IFN signaling pathway, opening additional avenues for preventing hyperactivation and maintaining immunity homeostasis. [10] Here, we found that retinoic acid-inducible gene I (RIG-I), a key cytosolic RNA sensor that recognizes RNA virus and initiates the MAVS-IRF3-type I IFN signaling cascade, is recruited to double-stranded breaks (DSBs) and suppresses non-homologous end joining (NHEJ). [11] Collectively, cGAS promotes the pathogenesis of SAE by up-regulating type I IFN signaling. [12] Several lines of evidence suggest that impaired type‐I IFN signaling may predispose to severe COVID‐19. [13] We show that DV-2 strategically tweaks STAT3 which is a negative regulator of Type I IFN signaling, in order to evade host Type I and Type III interferon response by upregulating its expression and activation. [14] RBN-2397 is a first-in class PARP7 inhibitor, which induces cancer cell autonomous and immune stimulatory effects in preclinical models through enhanced Type I IFN signaling in cancer cells. [15] In addition to selective loss of tissue-resident decidual macrophages, we report attenuation of antigen presentation and type I IFN signaling but upregulation of inflammatory cytokines and chemokines in blood monocyte derived decidual macrophages. [16] Aberrant type I IFN signaling, therefore, can exacerbate SLE by deregulated homeostasis leading to unnecessary persistence of the biological effects of type I IFNs. [17] Deficiency in type I IFN signaling was associated to an early and increased mortality, uncontrolled SLEV replication and impaired ISG expression, leading to increased proinflammatory cytokine production and brain pathology. [18] Further research showed that RACK1 inhibited the type I IFN signaling pathway during BEFV infection by degrading MAVS, and RACK1 degraded MAVS via the ubiquitin-proteasome system. [19] We have discovered that selective recruitment and activation of systemic CD8+ T cells into dMMR CRCs strictly depend on overexpression of CCL5 and CXCL10 due to endogenous activation of cGAS/STING and type I IFN signaling by damaged DNA. [20] However, in the absence of NS1, DDX3X promoted the formation of stress granules that facilitated efficient activation of type I IFN signaling. [21] The stimulator of interferon genes (STING) works as a critical nucleic acid sensor and adaptor in type I IFN signaling with possible implications in autoimmune diseases such as DM. [22] We found that ORF7b promoted expression of IFN-β, TNF-α, and IL-6, activated type-I IFN signaling through IRF3 phosphorylation, and activated TNFα-induced apoptosis in HEK293T cells and Vero E6 cells. [23] Blocking type I IFN signaling during E. [24] Analysis of the tumor microenvironment revealed a reduction in T-cell PD-1 expression, increased NK-cell granzyme B expression, and elevated type I IFN signaling in mice treated with the combination when compared with RT treatment alone. [25] Here, we developed a deterministic mathematical model based on the assumption that two cell subpopulations exist within the treated tumor: one population with high type I IFN signaling and immunogenicity and lower growth rate; the other population with low type I IFN signaling and immunogenicity and higher growth rate. [26] Our results reveal a novel mechanism underlying the infection-induced apoptosis that can be modulated by the NS1 and type I IFN signaling in IAV-infected cells. [27] Type I IFN signaling blockade rescued the Mtb-specific IFN-γ response and ameliorated lung immunopathology. [28] This study elucidates the novel role of DDX3X in regulating endogenous cellular dsRNA homeostasis and type I IFN signaling in breast cancer. [29] Mechanistically, upon the respiratory delivery, 2′3′-cGAMP was mainly internalized by alveolar macrophages, in which it activated the STING/IFN regulatory factor 3/type I IFN signaling axis to induce the production of inhibitory factors containing IFN-α, which blocked the IL-33–mediated activation of group 2 innate lymphoid (ILC2) cells in vivo. [30] In this study, we report the steady-state activation of type I IFN signaling and antiviral gene expression in CLPP-deficient cells and tissues, resulting in marked resistance to RNA and DNA virus infection. [31] Inhibition of oncogenic KIT in gastrointestinal stromal tumors decreases type I IFN signaling, impairing antigen presentation and diminishing CD8+ T-cell antitumor responses. [32] Collectively, these results indicate that during more than one TLR-ligand-induced immune signaling event, impairment of antiviral type I IFN response was restored by inhibition of MyD88 through MyD88-independent pathway of type I IFN signaling, thus, offer a MyD88-targeted approach for type I IFN induction. [33] • Therapeutic intervention of MyD88 also showed an increase in antiviral effect with strong type I IFN signaling linked to increased phosphorylation of IRFs via MyD88–independent pathway. [34] These observations uncover novel aspects of asbestos-induced mesothelioma whereby ERV expression increases due to promoter demethylation and is paralleled by increased levels of dsRNA and activation of type-I IFN signaling. [35] Neutralization of type I IFN signaling blocked noncognate intracellular production of IFN-γ. [36] Instead, their data showed that blockade of type I IFN signaling by anti– IFNα receptor 1 (anti– IFNAR1) decreases percentages and numbers of Tfh cells but increases production of immunoglobulin and autoantibodies in lupusprone mice. [37] These data collectively supported that MxA inhibits ZIKV replication through activation of the type I IFN signaling pathway. [38] The TM domain of MAVS governs the mitochondria localization of MAVS, and it is a key factor in type-I IFN signaling transduction via MAVS aggregation. [39] Interestingly, upregulation of NR_033736 itself is triggered by the type I IFN signaling. [40] Tumor-intrinsic type I IFN signaling initiated systemic STING-mediated antitumor inflammation and required CXCR3 expression. [41] The combination therapy enhanced phagocytosis of tumor cells and induced systemic anti-tumor immune responses, which rely on STING and type I IFN signaling. [42] SARS-CoV-2–specific T cells are protective and cross-reactive in vivo, and are shaped by type I IFN signaling. [43] Combination of anti-retroviral therapy (ART) and IFN-I receptor blockade therapy led to accelerated viral suppression and reduced latent HIV-1 reservoirs, suggesting that targeting type I IFN signaling can be used as a therapeutic strategy to alleviate T cell exhaustion. [44] Upregulated type I IFN signaling and constitutive expression of a subset of interferon-simulated genes (ISGs) play a major role in such resistance, while other mechanisms, such as inefficient viral attachment and resistance to VSV-mediated apoptosis, also play a role in some PDACs. [45] Type I IFN signaling genes were uniquely up-regulated in PBMCs infected with CHR strains, while genes involved in the immunological synapse were uniquely downregulated in SH infections. [46] show that selective inhibition of tyrosine kinase 2 (TYK2) can block potentially noxious type I IFN signaling but does not alter IFN-λ signaling, whereas the JAK1/2 inhibitor baricitinib blocks both types of IFN responses. [47] Oral dosing of the PARP7 small-molecule inhibitor, RBN-2397, results in complete tumor regression in a lung cancer xenograft and induces tumor-specific adaptive immune memory in an immunocompetent mouse cancer model, dependent on inducing type I IFN signaling in tumor cells. [48] The expression of type I IFN signaling components is markedly increased in psoriasis skin lesions. [49] Conclusion: We describe induction of ON in an animal model for NMOSD and show a requirement for type I IFN signaling in the disease process. [50]I형 IFN 신호전달의 억제는 PbT-II를 증가시키고 PbA 및 Pcc에 감염된 마우스 둘 다에서 PbT-II 세포의 Tfh 편향보다 Th1을 부분적으로 역전시켰다. [1] 그런 다음 인터페론 시뮬레이션 유전자(ISG) 세트가 I형 IFN 신호에 대한 응답으로 발현되어 세포를 항바이러스 상태로 설정합니다. [2] 여기에서 우리는 새로 확인된 자가포식 수용체인 CCDC50이 K63-폴리유비퀴틴화된 STING을 분해를 위해 자가용해소체에 전달함으로써 STING 유도 유형 I IFN 신호 활성을 조정한다고 보고합니다. [3] 167–175) 패혈성 쇼크가 있는 인간 환자의 DIC와 내피 세포(EC) 손상, 염증 및 섬유소 용해에 대한 I형 IFN 신호 전달의 잠재적인 핵심 역할을 확인합니다(2). [4] Apoptotic caspases는 최근에 비 감염성 컨텍스트와 바이러스 감염 중 유형 I IFN 신호 전달의 중요한 조절 인자로 등장했습니다. [5] 마우스에 다시 이식했을 때 내성 종양은 IL-6 억제(핵심 PTIS 구성요소)에 더 민감했으며 I형 IFN 신호전달이 차단되었을 때 성장이 현저히 감소했습니다. [6] ISG 및 I형 IFN 신호전달 경로 성분의 mRNA 및 단백질 발현은 정량적 실시간 중합효소 연쇄 반응, 웨스턴 블롯, 면역형광 및/또는 면역조직화학에 의해 평가되었다. [7] 이러한 결과는 AjIκBα가 NF-κB, AP1 및 I형 IFN 신호전달 경로의 활성화 억제를 통해 항균 및 항바이러스 감염에 대한 숙주의 선천 면역에서 중요한 음성 조절 기능을 함을 종합적으로 나타냅니다. [8] 유형 I IFN 신호가 분명히 새로운 메커니즘을 통해 Mtb에 감염된 대식세포의 죽음에 기여한다는 것을 발견했습니다. [9] 결론적으로, 이러한 발견은 hIFIT5가 I형 IFN 신호전달 경로에서 음성 조절자임을 나타내며, 이는 과활성화를 방지하고 면역 항상성을 유지하기 위한 추가 길을 열어줍니다. [10] 여기에서 우리는 RNA 바이러스를 인식하고 MAVS-IRF3-유형 I IFN 신호 전달 캐스케이드를 시작하는 주요 세포질 RNA 센서인 레티노산 유도성 유전자 I(RIG-I)이 이중 가닥 파손(DSB) 및 NHEJ(비상동 말단 접합)를 억제합니다. [11] 종합적으로, cGAS는 I형 IFN 신호전달을 상향 조절함으로써 SAE의 발병기전을 촉진한다. [12] 여러 증거에 따르면 손상된 I형 IFN 신호전달이 심각한 COVID-19에 걸리기 쉽습니다. [13] 우리는 DV-2가 발현 및 활성화를 상향 조절하여 호스트 유형 I 및 유형 III 인터페론 반응을 피하기 위해 유형 I IFN 신호의 음성 조절자인 STAT3를 전략적으로 조정한다는 것을 보여줍니다. [14] RBN-2397은 최초의 PARP7 억제제로, 암 세포에서 강화된 Type I IFN 신호전달을 통해 전임상 모델에서 암세포 자율 및 면역 자극 효과를 유도한다. [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23] nan [24] nan [25] nan [26] nan [27] I형 IFN 신호 전달 차단은 Mtb 특이적 IFN-γ 반응을 구출하고 폐 면역병리를 개선했습니다. [28] nan [29] nan [30] nan [31] nan [32] nan [33] nan [34] nan [35] nan [36] nan [37] nan [38] nan [39] nan [40] nan [41] nan [42] nan [43] nan [44] nan [45] I형 IFN 신호전달 유전자는 CHR 균주에 감염된 PBMC에서 독특하게 상향조절된 반면, 면역학적 시냅스에 관련된 유전자는 SH 감염에서 독특하게 하향조절되었다. [46] nan [47] nan [48] 유형 I IFN 신호 구성 요소의 발현은 건선 피부 병변에서 현저하게 증가합니다. [49] nan [50]
1 Ifn Signaling 1 Ifn 시그널링
Renitence induced by the TLR3 agonist Poly(I:C) was mediated in part by the type I IFN response, but renitence induced by Pam3CSK4 (TLR2/1), LPS (TLR4), IFNγ, or TNFα was independent of type 1 IFN signaling. [1] Results: Although QPD and XBD showed very little effect on the type 1 IFN signaling pathway in A549 cells, either QPD or XBD markedly inhibited the production of pro-inflammatory markers including interleukin-6, tumor necrosis factor-α, monocyte chemotactic protein-1, and chemokine ligand 10 in THP-1-derived M1 macrophages. [2] CDG-mediated suppression of type 2 inflammation occurred independent of IL-18R, IL-12, and STAT6 but required the stimulator of interferon genes (STING) and type 1 IFN signaling. [3] AUTHOR SUMMARY Type 1 IFN signaling in mammalian cells induces formation of the ISGF3 transcription factor complex, which binds to interferon stimulated response elements (ISREs) in the promoters of interferon stimulated genes (ISGs) in the cell nucleus. [4] The replication of mumps virus in PECs was inhibited by type 1 IFN signaling. [5] Type 1 IFN signaling in mammalian cells induces formation of the ISGF3 transcription factor complex, which binds to interferon stimulated response elements (ISREs) in the promoters of interferon-stimulated genes (ISGs) in the cell nucleus. [6] In these systems, we elucidate DNMTi/TAL potentiated cGAS-Sting and type 1 IFN signaling, culminating in the induction of IFN responsive genes and inflammatory cytokine production. [7]TLR3 작용제 Poly(I:C)에 의해 유도된 회복은 부분적으로 I형 IFN 반응에 의해 매개되었지만 Pam3CSK4(TLR2/1), LPS(TLR4), IFNγ 또는 TNFα에 의해 유도된 회복은 유형 1 IFN 신호전달과 무관했습니다. . [1] 결과: QPD와 XBD가 A549 세포에서 1형 IFN 신호 전달 경로에 거의 영향을 미치지 않았지만, QPD 또는 XBD는 인터루킨-6, 종양 괴사 인자-α, 단핵구 주화성 단백질-1을 포함한 전염증성 마커의 생성을 현저하게 억제했습니다. 및 THP-1 유래 M1 대식세포의 케모카인 리간드 10. [2] nan [3] nan [4] nan [5] nan [6] nan [7]
Mediated Ifn Signaling 중재된 Ifn 신호
In addition, butorphanol prevented the Toll/IL-1 receptor domain-containing adaptor inducing IFN-β (TRIF)-mediated IFN signaling pathway. [1] Furthermore, SARS-CoV-2 N inhibited polyinosinic: polycytidylic acid [poly(I:C)]-mediated IFN signaling at the level of Tank-binding kinase 1 (TBK1) and interfered with the association between TBK1 and interferon regulatory factor 3 (IRF3), subsequently preventing the nuclear translocation of IRF3. [2] These results indicate that bcIRF5 negatively regulates bcTBK1-mediated IFN signaling in healthy cells; however, it correlates with bcTBK1 and triggers cell death to inhibit the virus replication during the innate immune activation. [3] Based on our previous finding that bcTAK1 up‐regulates bcIRF7‐mediated IFN signaling during host innate immune activation, the data generated in this study support the conclusion that bcTAB1 interacts with bcTAK1 and boosts bcTAK1‐activated bcIRF7/IFN signaling during host antiviral innate immune response against GCRV and SVCV. [4]또한, 부토르파놀은 IFN-β(TRIF) 매개 IFN 신호 경로를 유도하는 Toll/IL-1 수용체 도메인 함유 어댑터를 방지했습니다. [1] 또한 SARS-CoV-2 N은 Tank-binding kinase 1(TBK1) 수준에서 polyinosinic: polycytidylic acid[poly(I:C)] 매개 IFN 신호 전달을 억제하고 TBK1과 인터페론 조절 인자 3 사이의 연관성을 방해했습니다. IRF3), 후속적으로 IRF3의 핵 전위를 방지합니다. [2] nan [3] nan [4]
Activate Ifn Signaling Ifn 시그널링 활성화
We used a chicken IRF7 (chIRF7) knockout DF-1 cell line in a series of experiments to demonstrate that chDDX1 activates IFN signaling via the chIRF7 pathway. [1] Stimulating innate immune cells to develop a proinflammatory tumor environment that activates IFN signaling and downstream adaptive antitumor immune mechanisms is predicted to overcome such resistance. [2] Significance The expression of numerous interferon (IFN)-inducible proteins is triggered by IFN or stimuli that activate IFN signaling pathways in innate immune responses. [3]우리는 chDDX1이 chIRF7 경로를 통해 IFN 신호를 활성화한다는 것을 입증하기 위해 일련의 실험에서 닭 IRF7(chIRF7) 녹아웃 DF-1 세포주를 사용했습니다. [1] IFN 신호 및 다운스트림 적응 항종양 면역 기전을 활성화하는 전염증성 종양 환경을 개발하기 위해 타고난 면역 세포를 자극하면 이러한 저항을 극복할 것으로 예상됩니다. [2] nan [3]
Ius Ifn Signaling Ius Ifn 시그널링
Gut transcriptomic analyses showed increased antiviral response mediated by pathways of type I/II IFN signaling, viral restriction factors, innate immunity, and B cell proliferation and provided the molecular signature underlying enhanced host immunity. [1] CONCLUSION Type II IFN signaling and STAT1 are associated with the pathogenesis of DADA2. [2] In vitro myeloid conversion did not require type I or type II IFN signaling. [3]장 전사체 분석은 I/II형 IFN 신호, 바이러스 제한 인자, 선천성 면역 및 B 세포 증식의 경로에 의해 매개되는 항바이러스 반응의 증가를 보여주었고 향상된 숙주 면역의 기초가 되는 분자 서명을 제공했습니다. [1] 결론 유형 II IFN 신호전달 및 STAT1은 DADA2의 발병기전과 관련이 있습니다. [2] nan [3]
Inhibit Ifn Signaling Ifn 시그널링 억제
This is in contrast to Middle East respiratory syndrome (MERS)-CoV, which effectively inhibits IFN signaling and OAS-RNase L and PKR pathways, but is similar to mutant MERS-CoV lacking innate immune antagonists. [1] Interestingly, HBx was reported to inhibit IFN signaling by targeting and downregulating mitochondrial antiviral-signaling protein. [2] JAK inhibitors are a promising therapy as they can inhibit IFN signaling, but further study is needed regarding which patients will benefit, dosing, and safety monitoring. [3]이는 IFN 신호 전달과 OAS-RNase L 및 PKR 경로를 효과적으로 억제하지만 선천적 면역 길항제가 없는 돌연변이 MERS-CoV와 유사한 중동 호흡기 증후군(MERS)-CoV와 대조적입니다. [1] 흥미롭게도 HBx는 미토콘드리아 항바이러스 신호 단백질을 표적으로 하고 하향 조절함으로써 IFN 신호를 억제하는 것으로 보고되었습니다. [2] nan [3]
Tonic Ifn Signaling 토닉 Ifn 시그널링
Profiling gut bacteria revealed a profound dysbiosis in absence of tonic IFN signaling, which triggered expansion of TH17 cells and loss of splenic Treg cells. [1] Profiling gut bacteria revealed a profound dysbiosis in the absence of tonic IFN signaling, which triggered expansion of TH17 cells and loss of splenic Treg cells. [2] Results Gene expression and DNA methylation analysis revealed that Echinaforce® treatment triggers antiviral innate immunity pathways, involving tonic IFN signaling, activation of pattern recognition receptors, chemotaxis and immunometabolism. [3]장내 세균의 프로파일링은 강장제 IFN 신호가 없는 상태에서 심각한 세균불균형을 드러냈고, 이는 TH17 세포의 확장과 비장 Treg 세포의 손실을 촉발했습니다. [1] 장내 세균을 프로파일링한 결과, TH17 세포의 확장과 비장 Treg 세포의 손실을 유발하는 강장제 IFN 신호가 없는 상태에서 심각한 미생물 불균형이 나타났습니다. [2] nan [3]
Host Ifn Signaling 호스트 Ifn 시그널링
Meanwhile, we discovered that the interaction of the CC1 domain of the Avibirnavirus VP3 protein and the residue lysine-155 of TRAF3 reduced the K33-linked polyubiquitination of TRAF3 and blocked the formation of the TRAF3-TBK1 complex, which contributed to the downregulation of host IFN signaling, supporting viral replication. [1] Our findings imply that Ranaviruses like FV3 have acquired previously unknown molecular mimics, interfering with host IFN signaling during evolution. [2] It also presents evidence implying that ranaviruses like FV3 have acquired previously unknown molecular mimics interfering with host IFN signaling during evolution. [3]한편, 우리는 Avibirnavirus VP3 단백질의 CC1 도메인과 TRAF3의 잔기 라이신-155의 상호작용이 TRAF3의 K33-연결된 폴리유비퀴틴화를 감소시키고 숙주의 하향 조절에 기여하는 TRAF3-TBK1 복합체의 형성을 차단한다는 것을 발견했습니다. IFN 신호 전달, 바이러스 복제 지원. [1] 우리의 발견은 FV3과 같은 라나바이러스가 이전에 알려지지 않은 분자 모방체를 획득하여 진화하는 동안 숙주 IFN 신호를 방해한다는 것을 의미합니다. [2] nan [3]
Iius Ifn Signaling
Here, we show that ORF6 inhibits the induction of innate immune signaling including upregulation of type I IFN upon viral infection, as well as type I and III IFN signaling. [1] SUMMARY Several new PIDs highlight the role of type I/III IFN signaling pathway, virus sensors, and host virus restriction factors in human antiviral immunity. [2]여기에서 우리는 ORF6이 바이러스 감염 시 I형 IFN의 상향 조절과 I형 및 III형 IFN 신호 전달을 포함하는 타고난 면역 신호의 유도를 억제한다는 것을 보여줍니다. [1] nan [2]
Regulate Ifn Signaling
Together, our data reveal that HCV infection results in the upregulation of miR-125a, which negatively regulates IFN signaling via inhibiting the expression of MAVS and TRAF6, thereby enabling the virus to evade innate antiviral immunity. [1] Here, using human and mouse cell lines along with gene microarrays, quantitative RT-PCR, viral infection and plaque assays, and reporter gene assays, we demonstrate that a microRNA cluster conserved among bilaterian animals, encoding miR-96, miR-182, and miR-183, regulates IFN signaling. [2]함께, 우리의 데이터는 HCV 감염이 MAVS 및 TRAF6의 발현을 억제함으로써 IFN 신호전달을 부정적으로 조절하는 miR-125a의 상향 조절을 초래하여 바이러스가 선천적 항바이러스 면역을 회피할 수 있게 함을 보여줍니다. [1] nan [2]
Induce Ifn Signaling Ifn 시그널링 유도
Overall, results indicate that ASFV CD2v activates NF-κB, which induces IFN signaling and apoptosis in swine lymphocytes/macrophages. [1] We found that the anti-CSFV effect of TNF was sensitive to JAK/STAT inhibitors, suggesting that TNF induces IFN signaling. [2]전반적으로 결과는 ASFV CD2v가 NF-κB를 활성화하여 돼지 림프구/대식세포에서 IFN 신호 및 세포자멸사를 유도함을 나타냅니다. [1] 본 발명자들은 TNF의 항-CSFV 효과가 JAK/STAT 억제제에 민감하다는 것을 발견하였고, 이는 TNF가 IFN 신호전달을 유도함을 시사한다. [2]
ifn signaling pathway Ifn 신호 전달 경로
The innate immune cGAS-STING-IFN signaling pathway exerts a critical role in sensing ASFV infection. [1] In addition, butorphanol prevented the Toll/IL-1 receptor domain-containing adaptor inducing IFN-β (TRIF)-mediated IFN signaling pathway. [2] BHRF1, a multifunctional viral protein expressed during Epstein-Barr virus reactivation, modulates mitochondrial dynamics and disrupts the IFN signaling pathway. [3] These results indicate that scopolamine hydrobromide contributes much to launch antiviral effects by remoulding the TLR and IFN signaling pathways that are involved in sensing and initiating the much-needed anti-JEV responses. [4] The mRNA and protein expressions of ISGs and type I IFN signaling pathway components were evaluated by quantitative real-time polymerase chain reaction, western blot, immunofluorescence, and/or immunohistochemistry. [5] By mapping the trajectory of intratumoral cDC1 maturation, we demonstrated the dynamic reprogramming of tumor-infiltrating cDC1s by NF-κB and IFN signaling pathways. [6] These results collectively indicated that AjIκBα function as an important negative regulation in innate immunity of host against antibacterial and antiviral infection likely via the inhibition of the activation of NF-κB, AP1, and type I IFN signaling pathways. [7] In conclusion, these findings indicate that hIFIT5 is a negative modulator in the type I IFN signaling pathway, opening additional avenues for preventing hyperactivation and maintaining immunity homeostasis. [8] Further research showed that RACK1 inhibited the type I IFN signaling pathway during BEFV infection by degrading MAVS, and RACK1 degraded MAVS via the ubiquitin-proteasome system. [9] Levels of two key IFN signaling pathway components, Tyk2 and STAT2, were significantly lower in SARS-CoV-2-infected cells. [10] Results: Although QPD and XBD showed very little effect on the type 1 IFN signaling pathway in A549 cells, either QPD or XBD markedly inhibited the production of pro-inflammatory markers including interleukin-6, tumor necrosis factor-α, monocyte chemotactic protein-1, and chemokine ligand 10 in THP-1-derived M1 macrophages. [11] Viperin_sv1, a novel viperin splice variant, has recently been identified from SVCV-infected FHM cells with a stronger antiviral effect than viperin by activating IFN signaling pathway. [12] These data collectively supported that MxA inhibits ZIKV replication through activation of the type I IFN signaling pathway. [13] We show that SARS-CoV-2 RNA activates the RIG-I-MAVS-dependent IFN signaling pathway. [14] Allicin treatment of infected Calu-3 cells reduced the expression of IFN signaling pathways and ISG effectors and reverted several host pathways to levels of uninfected cells. [15] Prior studies have mainly studied mixed alterations in the IFN signaling pathway in RA, but these studies have not been sufficient to elucidate how imbalanced IFN signaling subtly influences immune cells. [16] Here, we explore the diverse RNA regulatory mechanisms that modulate the innate antiviral immune response, with a focus on RNA sensing by RIG-I-like receptors (RLR), interferon (IFN) and IFN signaling pathways, viral pathogenesis, and host genetic variation that contributes to these processes. [17] Using unbiased proteomics, we identified that Linc-Pint associates with DDX24, which enables RIP1 to interact with IFN-regulatory factor 7 (IRF7) of the IFN signaling pathway. [18] More interestingly, inhibition of PIM1 kinase activity upregulated important downstream genes associated with antiviral responses that play crucial roles in the cellular type I IFN signaling pathway for antiviral activity (Supplementary Table). [19] Non-lesion and lesion NS-SE epidermis showed activation of the type I IFN signaling pathway, while lesion NS-ILC skin differed from non-lesion NS-ILC skin by increased complement activation and neutrophil infiltration. [20] Additionally, the type I IFN signaling pathway was not affected by NSP12, as demonstrated by the expression of interferon-stimulated genes (ISGs). [21] Loss of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes, and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 deficiency. [22] Functional analysis demonstrated that pathway and biological process involved in IFN signaling pathway, regulation of type 1 IFN production and response to IFN-γ. [23] Immune-related gene functions and pathways associated with these genes were evaluated, revealing that the type I IFN signaling pathway was the most significantly enriched pathway in our RNA-seq dataset, with 14 DEGs identified therein including ISG15, MX2, IRF9, IFIT3, IFIT2, OAS3, IFIT1, IFI6, OAS2, OASL, RSAD2, OAS1, IRF7, and MX1. [24] During disease course, interferon gamma response was upregulated; T/NK cell subtypes presented activation and exhaustion properties, which might be driven by monocytes through IL-1β signaling pathways; The proportion of plasma cells was increased, which might be driven by NK cells through IFN signaling pathways; Additionally, interferon gamma response was upregulated in sepsis secondary to pneumonia induced by SARS-COV-2 compared with that induced by influenza virus and bacteria. [25] Tumor necrosis factor receptor 1 (TNFR1) associated death domain protein (TRADD) is a pivotal adaptor in TNF signaling pathway and up-regulates MAVS/IFN signaling pathway in human and mammal. [26] Moreover, we present the current evidence showing that, in β-cells, type I IFN signaling pathway activation leads to several outcomes, such as long-lasting major histocompatibility complex (MHC) class I hyperexpression, endoplasmic reticulum (ER) stress, epigenetic changes, and induction of posttranscriptional as well as posttranslational modifications. [27] This paper summarizes the molecular mechanisms of hantavirus evasion mechanisms of the IFN signaling pathway and cellular processes such as regulated cell death and cell stress. [28] Significance The expression of numerous interferon (IFN)-inducible proteins is triggered by IFN or stimuli that activate IFN signaling pathways in innate immune responses. [29] SUMMARY Several new PIDs highlight the role of type I/III IFN signaling pathway, virus sensors, and host virus restriction factors in human antiviral immunity. [30] Furthermore, the Brucella-induced UPR is crucial for induction of multiple molecules linked to type I IFN signaling pathway, such as IFN-β, IFN regulatory factor 1, and guanylate-binding proteins. [31]타고난 면역 cGAS-STING-IFN 신호 전달 경로는 ASFV 감염을 감지하는 데 중요한 역할을 합니다. [1] 또한, 부토르파놀은 IFN-β(TRIF) 매개 IFN 신호 경로를 유도하는 Toll/IL-1 수용체 도메인 함유 어댑터를 방지했습니다. [2] Epstein-Barr 바이러스 재활성화 동안 발현되는 다기능 바이러스 단백질인 BHRF1은 미토콘드리아 역학을 조절하고 IFN 신호 전달 경로를 방해합니다. [3] 이러한 결과는 스코폴라민 하이드로브로마이드가 필요한 항-JEV 반응을 감지하고 개시하는 데 관여하는 TLR 및 IFN 신호 전달 경로를 재형성함으로써 항바이러스 효과를 시작하는 데 크게 기여한다는 것을 나타냅니다. [4] ISG 및 I형 IFN 신호전달 경로 성분의 mRNA 및 단백질 발현은 정량적 실시간 중합효소 연쇄 반응, 웨스턴 블롯, 면역형광 및/또는 면역조직화학에 의해 평가되었다. [5] 종양 내 cDC1 성숙의 궤적을 매핑함으로써 우리는 NF-κB 및 IFN 신호 전달 경로에 의한 종양 침윤 cDC1의 동적 재프로그래밍을 시연했습니다. [6] 이러한 결과는 AjIκBα가 NF-κB, AP1 및 I형 IFN 신호전달 경로의 활성화 억제를 통해 항균 및 항바이러스 감염에 대한 숙주의 선천 면역에서 중요한 음성 조절 기능을 함을 종합적으로 나타냅니다. [7] 결론적으로, 이러한 발견은 hIFIT5가 I형 IFN 신호전달 경로에서 음성 조절자임을 나타내며, 이는 과활성화를 방지하고 면역 항상성을 유지하기 위한 추가 길을 열어줍니다. [8] nan [9] nan [10] 결과: QPD와 XBD가 A549 세포에서 1형 IFN 신호 전달 경로에 거의 영향을 미치지 않았지만, QPD 또는 XBD는 인터루킨-6, 종양 괴사 인자-α, 단핵구 주화성 단백질-1을 포함한 전염증성 마커의 생성을 현저하게 억제했습니다. 및 THP-1 유래 M1 대식세포의 케모카인 리간드 10. [11] nan [12] nan [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23] nan [24] nan [25] nan [26] nan [27] nan [28] nan [29] nan [30] nan [31]
ifn signaling vium Ifn 시그널링 비움
Here, we aimed to determine whether IFN signaling via Janus kinase (JAK)/Signal transducers and activators of transcription (STAT) mediates dsRNA-induced responses in primary human VIC. [1] Double-strand breaks in mitochondrial DNA upregulated IFN signaling via cytosolic RNA sensing. [2] Together, our data reveal that HCV infection results in the upregulation of miR-125a, which negatively regulates IFN signaling via inhibiting the expression of MAVS and TRAF6, thereby enabling the virus to evade innate antiviral immunity. [3] We used a chicken IRF7 (chIRF7) knockout DF-1 cell line in a series of experiments to demonstrate that chDDX1 activates IFN signaling via the chIRF7 pathway. [4]여기에서 우리는 Janus 키나제(JAK)/신호 변환기 및 전사 활성화제(STAT)를 통한 IFN 신호전달이 1차 인간 VIC에서 dsRNA 유도 반응을 매개하는지 여부를 결정하는 것을 목표로 했습니다. [1] 미토콘드리아 DNA의 이중 가닥 파손은 세포질 RNA 감지를 통해 IFN 신호를 상향 조절했습니다. [2] 함께, 우리의 데이터는 HCV 감염이 MAVS 및 TRAF6의 발현을 억제함으로써 IFN 신호전달을 부정적으로 조절하는 miR-125a의 상향 조절을 초래하여 바이러스가 선천적 항바이러스 면역을 회피할 수 있게 함을 보여줍니다. [3] 우리는 chDDX1이 chIRF7 경로를 통해 IFN 신호를 활성화한다는 것을 입증하기 위해 일련의 실험에서 닭 IRF7(chIRF7) 녹아웃 DF-1 세포주를 사용했습니다. [4]
ifn signaling component Ifn 신호 구성 요소
The expression of type I IFN signaling components is markedly increased in psoriasis skin lesions. [1] Herein, we summarize the potential role of type I IFN signaling components as therapeutic targets. [2] We show that mice deficient in IFN signaling components including IFN alpha and beta receptor 1 (IFNAR1), interferon regulatory factor 1 (IRF1), IRF9, and STAT1 each have reduced bone density and increased osteoclastogenesis compared to wild type mice. [3]유형 I IFN 신호 구성 요소의 발현은 건선 피부 병변에서 현저하게 증가합니다. [1] 여기에서, 우리는 치료 표적으로서 I형 IFN 신호 성분의 잠재적인 역할을 요약합니다. [2] nan [3]
ifn signaling contribute
find that type I IFN signaling contributes to the death of Mtb-infected macrophages through an apparently novel mechanism. [1] In SLE, IFN-stimulated genes induced by IFN signaling contribute to a positive feedback loop of autoimmunity, resulting in perpetual autoimmune inflammation. [2]유형 I IFN 신호가 분명히 새로운 메커니즘을 통해 Mtb에 감염된 대식세포의 죽음에 기여한다는 것을 발견했습니다. [1] nan [2]
ifn signaling blockade
Type I IFN signaling blockade rescued the Mtb-specific IFN-γ response and ameliorated lung immunopathology. [1] Taken together, our study identifies a new mechanism by which a virus degrades STAT2 for IFN signaling blockade, highlighting the diversity of mechanisms employed by viruses to subvert the IFN response. [2]I형 IFN 신호 전달 차단은 Mtb 특이적 IFN-γ 반응을 구출하고 폐 면역병리를 개선했습니다. [1] nan [2]
ifn signaling cascade Ifn 시그널링 캐스케이드
Here, we found that retinoic acid-inducible gene I (RIG-I), a key cytosolic RNA sensor that recognizes RNA virus and initiates the MAVS-IRF3-type I IFN signaling cascade, is recruited to double-stranded breaks (DSBs) and suppresses non-homologous end joining (NHEJ). [1] Dysregulations of Type I IFN signaling cascade are more and more frequently found in the tumor microenvironment, representing critical determinants of therapeutic innate and adaptive resistance to several anticancer treatments. [2]여기에서 우리는 RNA 바이러스를 인식하고 MAVS-IRF3-유형 I IFN 신호 전달 캐스케이드를 시작하는 주요 세포질 RNA 센서인 레티노산 유도성 유전자 I(RIG-I)이 이중 가닥 파손(DSB) 및 NHEJ(비상동 말단 접합)를 억제합니다. [1] 유형 I IFN 신호 전달 캐스케이드의 조절 장애는 종양 미세 환경에서 점점 더 자주 발견되며, 이는 여러 항암 치료에 대한 치료적 선천성 및 적응 내성의 중요한 결정 요인을 나타냅니다. [2]
ifn signaling resolf Ifn 시그널링 해결
We also found that the subnuclear condensates, promyelocytic leukemia-nuclear bodies (PML-NBs), are absent from primary sympathetic and sensory neurons but form with type I IFN treatment and persist even when IFN signaling resolves. [1] We also find that the subnuclear condensates, promyelocytic leukemia nuclear bodies (PML‐NBs), are absent from primary sympathetic and sensory neurons but form with type I IFN treatment and persist even when IFN signaling resolves. [2]우리는 또한 subnuclear condensates, promyelocytic leukemia-nuclear bodys(PML-NBs)가 1차 교감 신경 및 감각 뉴런에는 없지만 I형 IFN 치료와 함께 형성되고 IFN 신호가 해결되는 경우에도 지속된다는 것을 발견했습니다. [1] 우리는 또한 핵내 응축물인 전골수구성 백혈병 핵체(PML-NB)가 1차 교감 및 감각 뉴런에 없지만 I형 IFN 치료로 형성되고 IFN 신호가 해결될 때에도 지속된다는 것을 발견했습니다. [2]
ifn signaling gene Ifn 신호전달 유전자
FOXA1 bound STAT2 DNA binding domain and suppressed STAT2 DNA binding activity, IFN signaling gene expression and cancer immune response independently of the transactivation activity of FOXA1 and its mutations detected in prostate and breast cancers. [1] Type I IFN signaling genes were uniquely up-regulated in PBMCs infected with CHR strains, while genes involved in the immunological synapse were uniquely downregulated in SH infections. [2]FOXA1은 STAT2 DNA 결합 도메인에 결합하고 전립선암 및 유방암에서 검출된 FOXA1의 전사활성화 활성 및 돌연변이와 독립적으로 STAT2 DNA 결합 활성, IFN 신호전달 유전자 발현 및 암 면역 반응을 억제했습니다. [1] I형 IFN 신호전달 유전자는 CHR 균주에 감염된 PBMC에서 독특하게 상향조절된 반면, 면역학적 시냅스에 관련된 유전자는 SH 감염에서 독특하게 하향조절되었다. [2]