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  1. Article ; Online: High-power polarization-maintaining LP

    Zhu, Qixin / Shi, Jianhong / Hu, Huixuan / Wu, Jie / Wang, Zhiyuan / Xing, Yinbing / Li, Jinyan / Yan, Dapeng / Li, Cheng

    Optics express

    2024  Volume 32, Issue 6, Page(s) 8862–8876

    Abstract: ... An ... ...

    Abstract An LP
    Language English
    Publishing date 2024-04-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1491859-6
    ISSN 1094-4087 ; 1094-4087
    ISSN (online) 1094-4087
    ISSN 1094-4087
    DOI 10.1364/OE.516635
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: SARS-COV-2 protein NSP9 promotes cytokine production by targeting TBK1.

    Zhang, Yihua / Xin, Bowen / Liu, Yinan / Jiang, Wenyi / Han, Wendong / Deng, Jian / Wang, Peihui / Hong, Xiaowu / Yan, Dapeng

    Frontiers in immunology

    2023  Volume 14, Page(s) 1211816

    Abstract: SARS-COV-2 infection-induced excessive or uncontrolled cytokine storm may cause injury of host tissue or even death. However, the mechanism by which SARS-COV-2 causes the cytokine storm is unknown. Here, we demonstrated that SARS-COV-2 protein NSP9 ... ...

    Abstract SARS-COV-2 infection-induced excessive or uncontrolled cytokine storm may cause injury of host tissue or even death. However, the mechanism by which SARS-COV-2 causes the cytokine storm is unknown. Here, we demonstrated that SARS-COV-2 protein NSP9 promoted cytokine production by interacting with and activating TANK-binding kinase-1 (TBK1). With an rVSV-NSP9 virus infection model, we discovered that an NSP9-induced cytokine storm exacerbated tissue damage and death in mice. Mechanistically, NSP9 promoted the K63-linked ubiquitination and phosphorylation of TBK1, which induced the activation and translocation of IRF3, thereby increasing downstream cytokine production. Moreover, the E3 ubiquitin ligase Midline 1 (MID1) facilitated the K48-linked ubiquitination and degradation of NSP9, whereas virus infection inhibited the interaction between MID1 and NSP9, thereby inhibiting NSP9 degradation. Additionally, we identified Lys59 of NSP9 as a critical ubiquitin site involved in the degradation. These findings elucidate a previously unknown mechanism by which a SARS-COV-2 protein promotes cytokine storm and identifies a novel target for COVID-19 treatment.
    MeSH term(s) Animals ; Mice ; COVID-19/complications ; COVID-19/genetics ; COVID-19/immunology ; COVID-19 Drug Treatment ; Cytokine Release Syndrome/etiology ; Cytokine Release Syndrome/genetics ; Cytokine Release Syndrome/immunology ; Cytokines ; Disease Models, Animal ; Immunity, Innate ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/immunology ; SARS-CoV-2/metabolism ; Signal Transduction ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Cytokines ; NSP9 protein, SARS-CoV-2 ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Tbk1 protein, mouse (EC 2.7.1.-) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2023-10-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1211816
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Helicobacter pylori

    He, Huan / Liu, Jing / Li, Liuyan / Qian, Gui / Hao, Doudou / Li, Manman / Zhang, Yihua / Hong, Xiaowu / Xu, Jianqing / Yan, Dapeng

    Journal of immunology (Baltimore, Md. : 1950)

    2021  Volume 206, Issue 6, Page(s) 1161–1170

    Abstract: Helicobacter ... ...

    Abstract Helicobacter pylori
    MeSH term(s) Animals ; Antigens, Bacterial/genetics ; Antigens, Bacterial/metabolism ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Disease Models, Animal ; Gastric Mucosa/immunology ; Gastric Mucosa/microbiology ; Gastric Mucosa/pathology ; HEK293 Cells ; HeLa Cells ; Helicobacter Infections/immunology ; Helicobacter Infections/microbiology ; Helicobacter Infections/pathology ; Helicobacter pylori/immunology ; Helicobacter pylori/metabolism ; Humans ; Immunity, Innate ; Lysine/metabolism ; Macrophages, Peritoneal ; Male ; Mice ; Mice, Transgenic ; Primary Cell Culture ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/metabolism ; RAW 264.7 Cells ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Signal Transduction/immunology ; TNF Receptor-Associated Factor 6/metabolism ; Transfection ; Ubiquitination/immunology
    Chemical Substances Antigens, Bacterial ; Bacterial Proteins ; Recombinant Proteins ; TNF Receptor-Associated Factor 6 ; TRAF6 protein, mouse ; cagA protein, Helicobacter pylori ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48) ; Ptpn6 protein, mouse (EC 3.1.3.48) ; Lysine (K3Z4F929H6)
    Language English
    Publishing date 2021-02-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2000234
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Glutamylation of an HIV-1 protein inhibits the immune response by hijacking STING.

    Qian, Gui / Zhang, Yihua / Liu, Yinan / Li, Manman / Xin, Bowen / Jiang, Wenyi / Han, Wendong / Wang, Yu / Tang, Xian / Li, Liuyan / Zhu, Lingyan / Sun, Tao / Yan, Bo / Zheng, Yongtang / Xu, Jianqing / Ge, Baoxue / Zhang, Zheng / Yan, Dapeng

    Cell reports

    2023  Volume 42, Issue 5, Page(s) 112442

    Abstract: Cyclic GMP-AMP synthase (cGAS) recognizes Y-form cDNA of human immunodeficiency virus type 1 (HIV-1) and initiates antiviral immune response through cGAS-stimulator of interferon genes (STING)-TBK1-IRF3-type I interferon (IFN-I) signalingcascade. Here, ... ...

    Abstract Cyclic GMP-AMP synthase (cGAS) recognizes Y-form cDNA of human immunodeficiency virus type 1 (HIV-1) and initiates antiviral immune response through cGAS-stimulator of interferon genes (STING)-TBK1-IRF3-type I interferon (IFN-I) signalingcascade. Here, we report that the HIV-1 p6 protein suppresses HIV-1-stimulated expression of IFN-I and promotes immune evasion. Mechanistically, the glutamylated p6 at residue Glu6 inhibits the interaction between STING and tripartite motif protein 32 (TRIM32) or autocrine motility factor receptor (AMFR). This subsequently suppresses the K27- and K63-linked polyubiquitination of STING at K337, therefore inhibiting STING activation, whereas mutation of the Glu6 residue partially reverses the inhibitory effect. However, CoCl
    MeSH term(s) Humans ; HIV-1/metabolism ; Signal Transduction ; Membrane Proteins/metabolism ; Nucleotidyltransferases/metabolism ; Immunity, Innate/genetics
    Chemical Substances Membrane Proteins ; Nucleotidyltransferases (EC 2.7.7.-)
    Language English
    Publishing date 2023-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112442
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: SHP-1 suppresses the antiviral innate immune response by targeting TRAF3.

    Hao, Doudou / Wang, Yu / Li, Liuyan / Qian, Gui / Liu, Jing / Li, Manman / Zhang, Yihua / Zhou, Ruixue / Yan, Dapeng

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2020  Volume 34, Issue 9, Page(s) 12392–12405

    Abstract: Type I interferons play a pivotal role in innate immune response to virus infection. The protein tyrosine phosphatase SHP-1 was reported to function as a negative regulator of inflammatory cytokine production by inhibiting activation of NF-κB and MAPKs ... ...

    Abstract Type I interferons play a pivotal role in innate immune response to virus infection. The protein tyrosine phosphatase SHP-1 was reported to function as a negative regulator of inflammatory cytokine production by inhibiting activation of NF-κB and MAPKs during bacterial infection, however, the role of SHP-1 in regulating type I interferons remains unknown. Here, we demonstrated that knockout or knockdown of SHP-1 in macrophages promoted both HSV-1- and VSV-induced antiviral immune response. Conversely, overexpression of SHP-1 in L929 cells suppressed the HSV-1- and VSV-induced immune response; suppression was directly dependent on phosphatase activity. We identified a direct interaction between SHP-1 and TRAF3; the association between these two proteins resulted in diminished recruitment of CK1ε to TRAF3 and inhibited its K63-linked ubiquitination; SHP-1 inhibited K63-linked ubiquitination of TRAF3 by promoting dephosphorylation at Tyr116 and Tyr446. Taken together, our results identify SHP-1 as a negative regulator of antiviral immunity and suggest that SHP-1 may be a target for intervention in acute virus infection.
    MeSH term(s) Animals ; HEK293 Cells ; Humans ; Immunity, Innate ; Mice ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/physiology ; RAW 264.7 Cells ; TNF Receptor-Associated Factor 3/physiology ; Ubiquitination ; Virus Diseases/immunology
    Chemical Substances TNF Receptor-Associated Factor 3 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48)
    Keywords covid19
    Language English
    Publishing date 2020-07-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202000600RR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Adaptive Surface Modeling of Soil Properties in Complex Landforms

    Liu, Wei / Zhang, Hai-Rong / Yan, Da-Peng / Wang, Sheng-Li

    ISPRS international journal of geo-information. 2017 June 20, v. 6, no. 6

    2017  

    Abstract: Spatial discontinuity often causes poor accuracy when a single model is used for the surface modeling of soil properties in complex geomorphic areas. Here we present a method for adaptive surface modeling of combined secondary variables to improve ... ...

    Abstract Spatial discontinuity often causes poor accuracy when a single model is used for the surface modeling of soil properties in complex geomorphic areas. Here we present a method for adaptive surface modeling of combined secondary variables to improve prediction accuracy during the interpolation of soil properties (ASM-SP). Using various secondary variables and multiple base interpolation models, ASM-SP was used to interpolate soil K+ in a typical complex geomorphic area (Qinghai Lake Basin, China). Five methods, including inverse distance weighting (IDW), ordinary kriging (OK), and OK combined with different secondary variables (e.g., OK-Landuse, OK-Geology, and OK-Soil), were used to validate the proposed method. The mean error (ME), mean absolute error (MAE), root mean square error (RMSE), mean relative error (MRE), and accuracy (AC) were used as evaluation indicators. Results showed that: (1) The OK interpolation result is spatially smooth and has a weak bull's-eye effect, and the IDW has a stronger ‘bull’s-eye’ effect, relatively. They both have obvious deficiencies in depicting spatial variability of soil K+. (2) The methods incorporating combinations of different secondary variables (e.g., ASM-SP, OK-Landuse, OK-Geology, and OK-Soil) were associated with lower estimation bias. Compared with IDW, OK, OK-Landuse, OK-Geology, and OK-Soil, the accuracy of ASM-SP increased by 13.63%, 10.85%, 9.98%, 8.32%, and 7.66%, respectively. Furthermore, ASM-SP was more stable, with lower MEs, MAEs, RMSEs, and MREs. (3) ASM-SP presents more details than others in the abrupt boundary, which can render the result consistent with the true secondary variables. In conclusion, ASM-SP can not only consider the nonlinear relationship between secondary variables and soil properties, but can also adaptively combine the advantages of multiple models, which contributes to making the spatial interpolation of soil K+ more reasonable.
    Keywords kriging ; landforms ; models ; potassium ; prediction ; soil properties ; watersheds ; China
    Language English
    Dates of publication 2017-0620
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2655790-3
    ISSN 2220-9964
    ISSN 2220-9964
    DOI 10.3390/ijgi6060178
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: High power all-fiber amplifier with different seed power injection.

    Wang, Jianming / Yan, Dapeng / Xiong, Songsong / Huang, Bao / Li, Cheng

    Optics express

    2016  Volume 24, Issue 13, Page(s) 14463–14469

    Abstract: We report a high power all-fiber amplifier with suitable seed power injected by an all-fiber laser. Different seed powers were injected into the all-fiber amplifier during our amplification experiments, and we found the stimulated Raman scattering (SRS) ... ...

    Abstract We report a high power all-fiber amplifier with suitable seed power injected by an all-fiber laser. Different seed powers were injected into the all-fiber amplifier during our amplification experiments, and we found the stimulated Raman scattering (SRS) threshold was inversely proportional to the injected seed power. More than 3 kW signal light with good beam quality (M<sup>2</sup> = 1.28) has been obtained with a suitable seed power injected, and the slope efficiency of the all-fiber amplifier was about 84.4%.
    Language English
    Publishing date 2016-06-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1491859-6
    ISSN 1094-4087 ; 1094-4087
    ISSN (online) 1094-4087
    ISSN 1094-4087
    DOI 10.1364/OE.24.014463
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Extracellular fibrinogen-binding protein released by intracellular Staphylococcus aureus suppresses host immunity by targeting TRAF3.

    Zhang, Xiaokai / Xiong, Tingrong / Gao, Lin / Wang, Yu / Liu, Luxuan / Tian, Tian / Shi, Yun / Zhang, Jinyong / Zhao, Zhuo / Lu, Dongshui / Luo, Ping / Zhang, Weijun / Cheng, Ping / Jing, Haiming / Gou, Qiang / Zeng, Hao / Yan, Dapeng / Zou, Quanming

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 5493

    Abstract: Many pathogens secrete effectors to hijack intracellular signaling regulators in host immune cells to promote pathogenesis. However, the pathogenesis of Staphylococcus aureus secretory effectors within host cells is unclear. Here, we report that ... ...

    Abstract Many pathogens secrete effectors to hijack intracellular signaling regulators in host immune cells to promote pathogenesis. However, the pathogenesis of Staphylococcus aureus secretory effectors within host cells is unclear. Here, we report that Staphylococcus aureus secretes extracellular fibrinogen-binding protein (Efb) into the cytoplasm of macrophages to suppress host immunity. Mechanistically, RING finger protein 114, a host E3 ligase, mediates K27-linked ubiquitination of Efb at lysine 71, which facilitates the recruitment of tumor necrosis factor receptor associated factor (TRAF) 3. The binding of Efb to TRAF3 disrupts the formation of the TRAF3/TRAF2/cIAP1 (cellular-inhibitor-of-apoptosis-1) complex, which mediates K48-ubiquitination of TRAF3 to promote degradation, resulting in suppression of the inflammatory signaling cascade. Additionally, the Efb K71R mutant loses the ability to inhibit inflammation and exhibits decreased pathogenicity. Therefore, our findings identify an unrecognized mechanism of Staphylococcus aureus to suppress host defense, which may be a promising target for developing effective anti-Staphylococcus aureus immunomodulators.
    MeSH term(s) Fibrinogen/metabolism ; Humans ; Lysine/metabolism ; Staphylococcal Infections ; Staphylococcus aureus/metabolism ; TNF Receptor-Associated Factor 2/metabolism ; TNF Receptor-Associated Factor 3/metabolism ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances TNF Receptor-Associated Factor 2 ; TNF Receptor-Associated Factor 3 ; TRAF3 protein, human ; Fibrinogen (9001-32-5) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Lysine (K3Z4F929H6)
    Language English
    Publishing date 2022-09-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-33205-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Imbalanced signal transduction in regulatory T cells expressing the transcription factor FoxP3.

    Yan, Dapeng / Farache, Julia / Mingueneau, Michael / Mathis, Diane / Benoist, Christophe

    Proceedings of the National Academy of Sciences of the United States of America

    2015  Volume 112, Issue 48, Page(s) 14942–14947

    Abstract: FoxP3(+) T regulatory (Treg) cells have a fundamental role in immunological tolerance, with transcriptional and functional phenotypes that demarcate them from conventional CD4(+) T cells (Tconv). Differences between these two lineages in the signaling ... ...

    Abstract FoxP3(+) T regulatory (Treg) cells have a fundamental role in immunological tolerance, with transcriptional and functional phenotypes that demarcate them from conventional CD4(+) T cells (Tconv). Differences between these two lineages in the signaling downstream of T-cell receptor-triggered activation have been reported, and there are different requirements for some signaling factors. Seeking a comprehensive view, we found that Treg cells have a broadly dampened activation of several pathways and signaling nodes upon TCR-mediated activation, with low phosphorylation of CD3ζ, SLP76, Erk1/2, AKT, or S6 and lower calcium flux. In contrast, STAT phosphorylation triggered by interferons, IL2 or IL6, showed variations between Treg and Tconv in magnitude or choice of preferential STAT activation but no general Treg signaling defect. Much, but not all, of the Treg/Tconv difference in TCR-triggered responses could be attributed to lower responsiveness of antigen-experienced cells with CD44(hi) or CD62L(lo) phenotypes, which form a greater proportion of the Treg pool. Candidate regulators were tested, but the Treg/Tconv differential could not be explained by overexpression in Treg cells of the signaling modulator CD5, the coinhibitors PD-1 and CTLA4, or the regulatory phosphatase DUSP4. However, transcriptome profiling in Dusp4-deficient mice showed that DUSP4 enhances the expression of a segment of the canonical Treg transcriptional signature, which partially overlaps with the TCR-dependent Treg gene set. Thus, Treg cells, likely because of their intrinsically higher reactivity to self, tune down TCR signals but seem comparatively more attuned to cytokines or other intercellular signals.
    MeSH term(s) Animals ; Antigens, CD/genetics ; Antigens, CD/immunology ; CTLA-4 Antigen/genetics ; CTLA-4 Antigen/immunology ; Calcium Signaling/genetics ; Calcium Signaling/immunology ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/immunology ; Gene Expression Regulation/immunology ; MAP Kinase Signaling System/genetics ; MAP Kinase Signaling System/immunology ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 3/genetics ; Mitogen-Activated Protein Kinase 3/immunology ; Programmed Cell Death 1 Receptor/genetics ; Programmed Cell Death 1 Receptor/immunology ; Protein Tyrosine Phosphatases/genetics ; Protein Tyrosine Phosphatases/immunology ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/immunology ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Antigens, CD ; CTLA-4 Antigen ; Ctla4 protein, mouse ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Receptors, Antigen, T-Cell ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; MKP2 protein, mouse (EC 3.1.3.48) ; Protein Tyrosine Phosphatases (EC 3.1.3.48)
    Language English
    Publishing date 2015-12-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1520393112
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: CCRL2 promotes antitumor T-cell immunity via amplifying TLR4-mediated immunostimulatory macrophage activation.

    Yin, Wei / Li, Yihong / Song, Yan / Zhang, Jiarui / Wu, Chao / Chen, Yu / Miao, Ying / Lin, Changdong / Lin, Yuli / Yan, Dapeng / Chen, Jianfeng / He, Rui

    Proceedings of the National Academy of Sciences of the United States of America

    2021  Volume 118, Issue 16

    Abstract: Macrophages are the key regulator of T-cell responses depending on their activation state. C-C motif chemokine receptor-like 2 (CCRL2), a nonsignaling atypical receptor originally cloned from LPS-activated macrophages, has recently been shown to regulate ...

    Abstract Macrophages are the key regulator of T-cell responses depending on their activation state. C-C motif chemokine receptor-like 2 (CCRL2), a nonsignaling atypical receptor originally cloned from LPS-activated macrophages, has recently been shown to regulate immune responses under several inflammatory conditions. However, whether CCRL2 influences macrophage function and regulates tumor immunity remains unknown. Here, we found that tumoral CCRL2 expression is a predictive indicator of robust antitumor T-cell responses in human cancers. CCRL2 is selectively expressed in tumor-associated macrophages (TAM) with immunostimulatory phenotype in humans and mice. Conditioned media from tumor cells could induce CCRL2 expression in macrophages primarily via TLR4, which is negated by immunosuppressive factors.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; China ; Female ; Immunization ; Macrophage Activation/immunology ; Macrophage Activation/physiology ; Male ; Melanoma/metabolism ; Mice ; NF-kappa B/metabolism ; Neoplasms/genetics ; Neoplasms/immunology ; Receptors, CCR/genetics ; Receptors, CCR/metabolism ; Signal Transduction ; T-Lymphocytes/metabolism ; Toll-Like Receptor 4/immunology ; Toll-Like Receptor 4/metabolism ; Tumor-Associated Macrophages/immunology ; Tumor-Associated Macrophages/metabolism
    Chemical Substances Ccrl2 protein, mouse ; NF-kappa B ; Receptors, CCR ; Tlr4 protein, mouse ; Toll-Like Receptor 4
    Language English
    Publishing date 2021-03-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2024171118
    Database MEDical Literature Analysis and Retrieval System OnLINE

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