| TRAM deletion attenuates monocyte exhaustion and alleviates sepsis severity. | TRAM deletion attenuates monocyte exhaustion and alleviates sepsis severity.
Wang J, Wu Y, Lin R, Zhang Y, Li L., Free PMC Article | 02/8/2024 |
| The role of TRIF protein in regulating the proliferation and antigen presentation ability of myeloid dendritic cells through the ERK1/2 signaling pathway in chronic low-grade inflammation of intestinal mucosa mediated by flagellin-TLR5 complex signal. | The role of TRIF protein in regulating the proliferation and antigen presentation ability of myeloid dendritic cells through the ERK1/2 signaling pathway in chronic low-grade inflammation of intestinal mucosa mediated by flagellin-TLR5 complex signal.
Zhuang Z, Chen Y, Zheng J, Chen S., Free PMC Article | 01/12/2024 |
| Pathogenic Leptospires Limit Dendritic Cell Activation Through Avoidance of TLR4 and TRIF Signaling. | Pathogenic Leptospires Limit Dendritic Cell Activation Through Avoidance of TLR4 and TRIF Signaling.
Cagliero J, Vernel-Pauillac F, Murray G, Adler B, Matsui M, Werts C., Free PMC Article | 07/16/2022 |
| TRAM-Related TLR4 Pathway Antagonized by IRAK-M Mediates the Expression of Adhesion/Coactivating Molecules on Low-Grade Inflammatory Monocytes. | TRAM-Related TLR4 Pathway Antagonized by IRAK-M Mediates the Expression of Adhesion/Coactivating Molecules on Low-Grade Inflammatory Monocytes.
Pradhan K, Geng S, Zhang Y, Lin RC, Li L., Free PMC Article | 01/8/2022 |
| Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance. | Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance.
Qin Y, Jia L, Liu H, Ma W, Ren X, Li H, Liu Y, Li H, Ma S, Liu M, Li P, Yan J, Zhang J, Guo Y, You H, Guo Y, Rahman NA, Wołczyński S, Kretowski A, Li D, Li X, Ren F, Li X., Free PMC Article | 12/11/2021 |
| SET8 participates in lipopolysaccharide-mediated BV2 cell inflammation via modulation of TICAM-2 expression. | SET8 participates in lipopolysaccharide-mediated BV2 cell inflammation via modulation of TICAM-2 expression.
Zhao Y, Yang X, Meng F, Li W. | 08/7/2021 |
| TICAM2-related pathway mediates neutrophil exhaustion. | TICAM2-related pathway mediates neutrophil exhaustion.
Lin R, Zhang Y, Pradhan K, Li L., Free PMC Article | 03/13/2021 |
| TRIF deficiency protects non-obese diabetic mice from type 1 diabetes by modulating the gut microbiota and dendritic cells. | TRIF deficiency protects non-obese diabetic mice from type 1 diabetes by modulating the gut microbiota and dendritic cells.
Gülden E, Chao C, Tai N, Pearson JA, Peng J, Majewska-Szczepanik M, Zhou Z, Wong FS, Wen L., Free PMC Article | 10/5/2019 |
| TLR3(-/-) and TRIF(-/-) mice presented higher parasite burdens, increased inflammatory lesions, and reduced production of interleukin 12p40, tumor necrosis factor, gamma interferon, and nitric oxide. | Toll-Like Receptor 3-TRIF Pathway Activation by Neospora caninum RNA Enhances Infection Control in Mice.
Miranda VDS, França FBF, da Costa MS, Silva VRS, Mota CM, Barros PDSC, Parreira KS, Santiago FM, Mineo JR, Mineo TWP., Free PMC Article | 08/31/2019 |
| Analysis of NF-kappaB activation caused by transient expression of proteins involved in the MyD88-dependent pathway in TLR signaling revealed that AKT1 suppressed signaling that occurs between activation of IKKbeta and that of NF-kappaB. | AKT1 distinctively suppresses MyD88-depenedent and TRIF-dependent Toll-like receptor signaling in a kinase activity-independent manner.
Zenke K, Muroi M, Tanamoto KI. | 05/18/2019 |
| TRIF is a downstream protein of TLRs receptors which play a vital role in innate immunity. Expression of TRIF is downregulated in hyperthermia along with inactivation of NF-kappaB pathway. | Ultrasound hyperthermia enhances chemo-sensitivity in oral squamous cell carcinoma by TRIF-mediated pathway.
Ju H, Mao L, Zhang L, Liu S, Wu Y, Ruan M, Hu J, Ren G. | 03/16/2019 |
| These data suggest that IPS-1 plays a more important role than TRIF in the early type I IFN response and that both IPS-1 and TRIF are involved at later stages of Zika virus infection. | Predominant role of IPS-1 over TRIF adaptor proteins in early innate immune response against Zika virus in mice.
Piret J, Carbonneau J, Rhéaume C, Baz M, Boivin G. | 03/9/2019 |
| Experiments with homozygous knockouts of Irakm (encoding a suppressor of MyD88 inactivation) and Trif in competitive bone marrow transplants revealed that MyD88 is required for High Fat Diet expansion of granulocyte macrophage progenitors and that Trif is required for pregranulocyte macrophage progenitor expansion. | TLR4, TRIF, and MyD88 are essential for myelopoiesis and CD11c(+) adipose tissue macrophage production in obese mice.
Griffin C, Eter L, Lanzetta N, Abrishami S, Varghese M, McKernan K, Muir L, Lane J, Lumeng CN, Singer K., Free PMC Article | 01/26/2019 |
| Using ovalbumin as model antigen, the authors showed that exposure of dendritic cells to hyperosmolarity strongly inhibits activation of antigen-specific T cells despite enhancement of antigen uptake, processing and presentation. They identified TRIF as key mediator of this phenomenon. | Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner.
Popovic ZV, Embgenbroich M, Chessa F, Nordström V, Bonrouhi M, Hielscher T, Gretz N, Wang S, Mathow D, Quast T, Schloetel JG, Kolanus W, Burgdorf S, Gröne HJ., Free PMC Article | 09/8/2018 |
| the present study indicated that MyD88 and TRIF blockades serve notable and equivalent roles in protecting cardiac deterioration from severe sepsis by attenuating cytokine release, reducing neutrophil infiltration and alleviating apoptosis. | The inhibition of MyD88 and TRIF signaling serve equivalent roles in attenuating myocardial deterioration due to acute severe inflammation.
Ouyang MZ, Zhou D, Zhu Y, Zhang M, Li L. | 07/14/2018 |
| lipopolysaccharide (LPS) application induces proliferation of dormant hematopoietic stem cells (HSC) and impairs HSC self-renewal via TLR4-TRIF-ROS-p38 signaling. | Pathogen-Induced TLR4-TRIF Innate Immune Signaling in Hematopoietic Stem Cells Promotes Proliferation but Reduces Competitive Fitness.
Takizawa H, Fritsch K, Kovtonyuk LV, Saito Y, Yakkala C, Jacobs K, Ahuja AK, Lopes M, Hausmann A, Hardt WD, Gomariz Á, Nombela-Arrieta C, Manz MG. | 04/28/2018 |
| These results indicate a critical role for Ticam2 in SARS-CoV disease, and highlight the importance of host genetic variation in disease responses. | Allelic Variation in the Toll-Like Receptor Adaptor Protein Ticam2 Contributes to SARS-Coronavirus Pathogenesis in Mice.
Gralinski LE, Menachery VD, Morgan AP, Totura AL, Beall A, Kocher J, Plante J, Harrison-Shostak DC, Schäfer A, Pardo-Manuel de Villena F, Ferris MT, Baric RS., Free PMC Article | 03/31/2018 |
| Distinct mechanisms downstream of TLR4 signaling mediate myelosuppression and hematopoietic stem cell exhaustion during sepsis through unique effects of MyD88 and TRIF. | Sepsis Induces Hematopoietic Stem Cell Exhaustion and Myelosuppression through Distinct Contributions of TRIF and MYD88.
Zhang H, Rodriguez S, Wang L, Wang S, Serezani H, Kapur R, Cardoso AA, Carlesso N., Free PMC Article | 11/18/2017 |
| these data show that both Myd88 and TRIF are necessary for Th17 differentiation in the lungs in response to immunization with lipopolysaccharide | Cytokine regulation of lung Th17 response to airway immunization using LPS adjuvant.
Caucheteux SM, Hu-Li J, Mohammed RN, Ager A, Paul WE., Free PMC Article | 11/11/2017 |
| these studies reveal an additional regulatory function of TRIM8 in innate immune responses: TRIM8 catalyzes polyubiquitination of TRIF, resulting in disruption of TRIF-TBK1 interaction | TRIM8 Negatively Regulates TLR3/4-Mediated Innate Immune Response by Blocking TRIF-TBK1 Interaction.
Ye W, Hu MM, Lei CQ, Zhou Q, Lin H, Sun MS, Shu HB. | 09/30/2017 |
| Stimulation of the TLR4-TRIF pathway can protect against the development of allergic airway disease and that a TRIF-dependent adjuvant effect on CD4(+) ICOS(+) T-cell responses may be a contributing mechanism. | The TLR4-TRIF pathway can protect against the development of experimental allergic asthma.
Shalaby KH, Al Heialy S, Tsuchiya K, Farahnak S, McGovern TK, Risse PA, Suh WK, Qureshi ST, Martin JG., Free PMC Article | 09/23/2017 |
| Monophosphoryl lipid A stimulation of a TLR4-TRIF-PI3K-Akt pathway prevents lipopolysaccharide-induced ERK activation in the medullar thick ascending limb. | Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through a TLR4-TRIF-PI3K signaling pathway.
Watts BA 3rd, George T, Sherwood ER, Good DW., Free PMC Article | 09/23/2017 |
| study reporst a key role for TNF/TNFR1 in Yersinia-induced cell death of murine macrophages, which occurs despite the blockade of NF-kappaB and MAPK signaling imposed by Yersinia on infected cells | Cell-Extrinsic TNF Collaborates with TRIF Signaling To Promote Yersinia-Induced Apoptosis.
Peterson LW, Philip NH, Dillon CP, Bertin J, Gough PJ, Green DR, Brodsky IE., Free PMC Article | 08/12/2017 |
| STING and TRIF Contribute to Mouse Sepsis, Depending on Severity of the Disease Model | STING and TRIF Contribute to Mouse Sepsis, Depending on Severity of the Disease Model.
Heipertz EL, Harper J, Walker WE. | 07/1/2017 |
| the role of Toll-like receptor (TLR) 2, TLR4, myeloid differentiation response gene 88, and Toll-IL-1 receptor domain-containing adaptor-inducing interferon-gamma (TRIF), factors critically involved in the TLR signaling pathway, was studied in experimental autoimmune neuritis. | Toll-Like Receptor 2, Toll-Like Receptor 4, Myeloid Differentiation Response Gene 88, and Toll-IL-1 Receptor Domain-Containing Adaptor-Inducing Interferon-γ (TRIF) Selectively Regulate Susceptibility of P0(106-125)-Induced Murine Experimental Autoimmune Neuritis.
Brunn A, Mihelcic M, Carstov M, Feind L, Wieser EC, Schmidt J, Utermöhlen O, Deckert M. | 05/27/2017 |