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Добірка наукової літератури з теми "Siglec-E"

Автор: Grafiati
Опубліковано: 10 січня 2023
Оновлено: 28 січня 2023

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Статті в журналах з теми "Siglec-E"

1

Schmassmann, Philip, Tomás A. Martins, Michal Stanczak, Marie-Françoise Ritz, Tala Shekarian, Marta McDaid, Heinz Läubli, and Gregor Hutter. "EXTH-45. MICROGLIA-SPECIFIC DISRUPTION OF SIALIC ACID-SIGLEC-9/E INTERACTIONS: A NOVEL IMMUNOTHERAPY AGAINST GLIOBLASTOMA?" Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi173. http://dx.doi.org/10.1093/neuonc/noab196.684.

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Анотація:
Abstract Recently, ‘don’t eat me’-signals like CD47 have emerged as novel innate immune checkpoints, enabling cancer cells to evade clearance by phagocytes such as monocyte-derived macrophages (MDM) or microglia (MG). Here, we aim at defining the role of inhibitory Siglec-9 in human and its mouse homologue Siglec-E in MG-centered immunotherapy against GBM. TCGA RNA-sequencing data revealed a significant correlation between high expression of immunoinhibitory SIGLEC9 and poor survival in GBM patients (log-rank p = 0.02). Siglec-E blockade increased murine MG mediated GBM cell in vitro phagocytosis (normalized phagocytosis of 1.00 in isotype vs. 1.76 in anti-Siglec-E antibody, p < 0.001). By employing a CT-2A orthotopic GBM mouse model with MG-specific spatio-temporal deletion of Siglece (Sall1 CreERT2 x Siglece flox ), we observed high MG-proliferation upon Siglec-E knockdown (Ki-67+ MG 14.8% in Cre- vs. 34.9% in Cre+, p < 0.0001) accompanied by an enhanced microglial GBM-cell uptake (5.6% in Cre- vs. 12.3% in Cre+, p < 0.001). This beneficial response was counteracted by an accentuated influx of pro-tumorigenic MDM in the Cre+ group (CD163high CD86low MDM of total MDM 47.1% in Cre- vs. 65.3% in Cre+, p = 0.002), which prevented an efficient adaptive anti-tumor immune response and survival benefit. Currently, we are investigating the cross-talk between GBM-associated MG and MDM upon Siglec-E knockdown by scRNAseq of the tumor-infiltrating immune compartment, including TCR-clonotype tracking. By genetically targeting sialic acids, the ligand for Siglec receptors, on CT-2A cells (GNE-KO), we observed a strong innate and adaptive immune response with less exhausted tumor-infiltrating CD8+ T-cells (14.8% in WT vs. 5.9% in GNE-KO, p = 0.003), which resulted in a prolonged survival (30d in WT vs. 41d post-tumor-injection in GNE-KO, p = 0.03). These data identify the sialic-acid-Siglec-E pathway as an anti-phagocytic signal in a pre-clinical GBM model, and demonstrate its therapeutic potential in GBM immunotherapy.
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2

Schmassmann, P., J. Roux, T. A. Martins, M. Ritz, T. Shekarian, M. McDaid, and H. Läubli G. Hutter. "PL02.2.A Microglia-specific disruption of sialic acid-Siglec-9/E interactions. A novel immunotherapy against glioblastoma?" Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii2. http://dx.doi.org/10.1093/neuonc/noac174.005.

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Анотація:
Abstract Background Recently, ‘don’t eat me’-signals like CD47 have emerged as novel innate immune checkpoints, enabling cancer cells to evade clearance by phagocytes such as monocyte-derived macrophages (MdM) or microglia (MG). Here, we aim at defining the role of inhibitory Siglec-9 in human and its mouse homologue Siglec-E in MG-centered immunotherapy against GBM. Material and Methods We employed a CT-2A orthotopic GBM mouse model with MG specific (Sall1CreERT2 x Sigleceflox) and whole innate-compartment (Cx3cr1CreERT2 x Sigleceflox) spatio-temporal deletion of Siglece. We applied multi-color flow cytometry, transcriptomics and proteomics analysis to decipher the immune response upon Siglece knockout. Results TCGA RNA-sequencing data revealed a significant correlation between high expression of immunoinhibitory SIGLEC9 and poor survival in GBM patients (log-rank p = 0.02). Siglec-E blockade increased murine MG mediated GBM cell in vitro phagocytosis (normalized phagocytosis of 1.00 in isotype vs. 1.76 in anti-Siglec-E antibody, p < 0.001). In the MG specific spatio-temporal deletion of Siglece (Sall1CreERT2 xSigleceflox), we observed high MG-proliferation upon Siglec-E knockout (Ki-67+ MG 14.8% in Cre- vs. 34.9% in Cre+, p < 0.0001) accompanied by an enhanced microglial GBM-cell uptake (5.6% in Cre- vs. 12.3% in Cre+, p < 0.001). By extending the Siglece knockout to the MdM compartment in our glioma mouse model (Cx3cr1CreERT2 x Sigleceflox) we observed a significantly prolonged survival in the Cx3cr1Cre+ population (21d in Cre- vs. 27d post-tumor injection in Cre+, p = 0.018), which could be further promoted by combining Siglece knockout with CD47 blockade (30d post-tumor injection in Cre+ + anti-CD47). Unbiased proteomics analysis revealed increased antigen processing and presentation capabilities of Siglece knockout MdMs which was confirmed by ex-vivo OT-1 cross-presentation assays. This bridging of innate and adaptive responses with increased T cell priming upon MdM Siglece knockout was further promoted by addition of anti-PD1 antibody to the combined Siglece knockout and anti-CD47 treatment arm. Animals harboring CT-2A tumors, exhibited a sustained survival benefit under the triple therapy, with 23% of animals experiencing long-term remission, even after tumor re-challenge into the contra-lateral hemisphere. By genetically targeting sialic acids, the ligand for Siglec receptors, on CT-2A cells (GNE-KO), we observed a strong innate and adaptive immune response with increased GBM-cell phagocytosis by MG and MdMs and less exhausted tumor-infiltrating CD8+ T-cells (14.8% in WT vs. 5.9% in GNE-KO, p = 0.003). Conclusion These data identify the sialic-acid-Siglec-E pathway as an anti-phagocytic signal in a pre-clinical GBM model, and demonstrate its therapeutic potential in GBM immunotherapy.
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3

Siddiqui, Shoib Sarwar, Rachel Matar, Maxime Merheb, Rawad Hodeify, Cijo George Vazhappilly, John Marton, Syed Azharuddin Shamsuddin, and Hussain Al Zouabi. "Siglecs in Brain Function and Neurological Disorders." Cells 8, no. 10 (September 22, 2019): 1125. http://dx.doi.org/10.3390/cells8101125.

Повний текст джерела
Анотація:
Siglecs (Sialic acid-binding immunoglobulin-type lectins) are a I-type lectin that typically binds sialic acid. Siglecs are predominantly expressed in immune cells and generate activating or inhibitory signals. They are also shown to be expressed on the surface of cells in the nervous system and have been shown to play central roles in neuroinflammation. There has been a plethora of reviews outlining the studies pertaining to Siglecs in immune cells. However, this review aims to compile the articles on the role of Siglecs in brain function and neurological disorders. In humans, the most abundant Siglecs are CD33 (Siglec-3), Siglec-4 (myelin-associated glycoprotein/MAG), and Siglec-11, Whereas in mice the most abundant are Siglec-1 (sialoadhesin), Siglec-2 (CD22), Siglec-E, Siglec-F, and Siglec-H. This review is divided into three parts. Firstly, we discuss the general biological aspects of Siglecs that are expressed in nervous tissue. Secondly, we discuss about the role of Siglecs in brain function and molecular mechanism for their function. Finally, we collate the available information on Siglecs and neurological disorders. It is intriguing to study this family of proteins in neurological disorders because they carry immunoinhibitory and immunoactivating motifs that can be vital in neuroinflammation.
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4

Schmassmann, Philip, Julien Roux, Nazanin Tatari, Tomas A. Martins, Marie-Françoise Ritz, Tala Shekarian, Heinz Laeubli, and Gregor Hutter. "EXTH-26. MICROGLIA-SPECIFIC DISRUPTION OF SIALIC ACID-SIGLEC-9/E INTERACTIONS: A NOVEL IMMUNOTHERAPY AGAINST GLIOBLASTOMA?" Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii215. http://dx.doi.org/10.1093/neuonc/noac209.825.

Повний текст джерела
Анотація:
Abstract Recently, ‘don’t eat me’-signals like CD47 have emerged as novel innate immune checkpoints, enabling cancer cells to evade clearance by phagocytes such as microglia (MG) or monocyte-derived cells (MdCs). Here, we aim at defining the role of inhibitory Siglec-9 in human and its mouse homologue Siglec-E in innate-centered immunotherapy against GBM. TCGA RNA-sequencing data revealed a significant correlation between high expression of immunoinhibitory SIGLEC9 and poor survival in GBM patients (log-rank p = 0.02). Using a CT-2A orthotopic GBM mouse model with MG-specific spatio-temporal deletion of Siglece (Sall1CreERT2 x Sigleceflox) , we observed high MG-proliferation upon Siglece knockout (Ki-67+ MG 14.8% in Crenegvs. 34.9% in Creposp < 0.0001) accompanied by an enhanced microglial GBM-cell uptake (5.6% in Crenegvs. 12.3% in Crepos, p < 0.001). By extending the Siglece knockout to the MdC compartment (Cx3cr1CreERT2x Sigleceflox) we observed a significantly prolonged survival in the Crepospopulation (21d in Crenegvs. 27d post-tumor injection in Crepos, p = 0.018), which could be further promoted by combining Siglece knockout with CD47 blockade (11% long-term remission in Crepos+ anti-CD47). Proteomics analysis revealed increased antigen processing and presentation capabilities of SigleceKOMdCs which was confirmed by ex-vivo OT-1 cross-presentation assays. This increased T cell priming upon MdC SigleceKOwas further boosted by addition of anti-PD1 antibody to the SigleceKO+ anti-CD47 combination. Resulting in 23% of animals experiencing long-term remission in the triple treatment arm, even after tumor re-challenge. Genetic targeting of sialic acids, the ligand for Siglec receptors, on CT-2A cells (GNE-KO), resulted in increased GBM-cell phagocytosis by MG and MdCs and less exhausted tumor-infiltrating CD8+ T cells (14.8% in WT vs. 5.9% in GNE-KO, p = 0.003). In a translational approach, we are currently testing anti-Siglec-9 treatment regimens in patient GBM explants, cultured for 5 days in perfusion bioreactors.
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5

Maniaci, Brandon Lee, David Friedman, Sydney Crotts, Matthew Rajcula, Keith Theodore, Hyun Se Kim Lee, and Virginia Shapiro. "Accelerated tumorigenesis in a colorectal cancer model in Siglec-E knockout mice." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 61.02. http://dx.doi.org/10.4049/jimmunol.208.supp.61.02.

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Анотація:
Abstract The lifetime risk for colorectal cancer in the United States is approximately 4%. Individuals with Inflammatory Bowel Disease, including Ulcerative Colitis and Crohn’s Disease, have a substantially increased risk of developing colorectal cancer. The mechanisms for accelerated tumorigenesis due to enhanced inflammation are not fully characterized. Siglecs (sialic acid immunoglobulin lectin-like proteins) are a family of inhibitory receptors that are negative regulators of the immune response. Siglec-E is an inhibitory receptor that is expressed by innate immune cells, including monocytes, macrophages, neutrophils and dendritic cells. Interestingly, mice deficient in Siglec-E have accelerated development of tumors and reduced survival in a spontaneous mouse model of colorectal cancer (TS4-cre LSL-KRasG12D APClox468/wt). While tumors develop at approximately 6 months in mice with Siglec-E, tumors develop at approximately two months in Siglec-E knockout mice. Initial results indicate that Siglec-E knockout mice also have accelerated gut inflammation using the DSS colitis model as compared to WT mice. Current studies are examining inflammation that develops during tumorigenesis in Siglec-E knockout mice.
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6

YU, Zhenbao, Meryem MAOUI, Liangtang WU, Denis BANVILLE, and Shi-Hsiang SHEN. "mSiglec-E, a novel mouse CD33-related siglec (sialic acid-binding immunoglobulin-like lectin) that recruits Src homology 2 (SH2)-domain-containing protein tyrosine phosphatases SHP-1 and SHP-2." Biochemical Journal 353, no. 3 (January 25, 2001): 483–92. http://dx.doi.org/10.1042/bj3530483.

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Анотація:
The sialic acid-binding immunoglobulin-like lectins (siglecs) represent a recently defined distinct subset of the immunoglobulin superfamily. By using the Src homology 2 (SH2)-domain-containing protein tyrosine phosphatase SHP-1 as bait in a yeast two-hybrid screen, we have identified a new member of the mouse siglec family, mSiglec-E. The mSiglec-E cDNA encodes a protein of 467 amino acids that contains three extracellular immunoglobulin-like domains, a transmembrane region and a cytoplasmic tail bearing two immunoreceptor tyrosine-based inhibitory motifs (ITIMs). mSiglec-E is highly expressed in mouse spleen, a tissue rich in leucocytes. The ITIMs of mSiglec-E can recruit SHP-1 and SHP-2, two inhibitory regulators of immunoreceptor signal transduction. This suggests that the function of mSiglec-E is probably an involvement in haematopoietic cells and the immune system as an inhibitory receptor. When expressed in COS-7 cells, mSiglec-E was able to mediate sialic acid-dependent binding to human red blood cells, suggesting that mSiglec-E may function through cell–cell interactions. In comparison with the known members of the siglec family, mSiglec-E exhibits a high degree of sequence similarity to both human siglec-7 and siglec-9. The gene encoding mSiglec-E is localized in the same chromosome as that encoding mouse CD33. Phylogenetic analysis reveals that neither mouse mSiglec-E nor CD33 shows a clear relationship with any human siglecs so far identified.
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7

Ibarlucea-Benitez, Itziar, Polina Weitzenfeld, Patrick Smith, and Jeffrey V. Ravetch. "Siglecs-7/9 function as inhibitory immune checkpoints in vivo and can be targeted to enhance therapeutic antitumor immunity." Proceedings of the National Academy of Sciences 118, no. 26 (June 21, 2021): e2107424118. http://dx.doi.org/10.1073/pnas.2107424118.

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Анотація:
Given the role of myeloid cells in T cell activation and in the antitumor response, targeting checkpoint molecules expressed on this population represents a promising strategy to augment antitumor immunity. However, myeloid checkpoints that can be effectively used as immunotherapy targets are still lacking. Here, we demonstrate the therapeutic potential of targeting the myeloid receptors Siglec-7 and Siglec-9 in vivo. By using a humanized immunocompetent murine model, we demonstrate that human Siglec-7 and Siglec-9, in addition to the murine homolog Siglec-E, inhibit the endogenous antitumor immune response, as well as the response to tumor-targeting and immune checkpoint inhibiting antibodies in vivo. The impact of these Siglecs on tumor progression is highly dependent on the anatomical distribution of the tumor and, as a consequence, the local tumor microenvironment, as tumors with a more immune-suppressive tumor microenvironment are less sensitive to Siglec perturbation. Finally, to assess the potential of these two receptors as targets for immunotherapy, we developed Fc engineered blocking antibodies to Siglec-7 and Siglec-9 and demonstrate that Siglec-7 and Siglec-9 blockade can significantly reduce tumor burden in vivo, demonstrating the therapeutic potential of targeting these two receptors.
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8

Lund, Sean J., Kathryn A. Patras, Jacqueline M. Kimmey, Asami Yamamura, Lindsay D. Butcher, Pamela G. B. Del Rosario, Gilberto E. Hernandez, et al. "Developmental immaturity of sialic acid recognition mediates neonatal susceptibility to GBS pneumonia." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 231.31. http://dx.doi.org/10.4049/jimmunol.204.supp.231.31.

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Abstract Group B Streptococcus (GBS) is a major neonatal pathogen but rarely causes disease in adults. We previously showed in mice that GBS escapes killing in the neonatal lung via its heavily sialylated capsule. Immune cells detect sialic acid moieties via expression of a repertoire of Siglec receptors. Combinatory expression of proinflammatory and anti-inflammatory Siglec receptors allows differentiation between host and pathogenic microbial sialic acid modifications. We test here the hypothesis that neonatal alveolar macrophages (AMs) fail to detect and kill GBS due to developmental immaturity of Siglec receptor expression. Adult AMs express the proinflammatory sialic acid receptor Sialoadhesin (Sn, Siglec-1) and the anti-inflammatory receptors Siglec-E and Siglec-F. However, real time PCR, immunofluorescence, and FACS detected only Siglec-E in neonatal lung macrophage populations. Sn expression increased soon after birth and was restricted to AMs. The timing of increased Sn expression in newborn mice correlated with susceptibility to GBS. Mice infected with GBS on day 1 suffered early onset mortality, while mice infected on day 2 displayed late onset disease. Mice infected on day 3 survived GBS infection. Further implicating AM immaturity, Csf2−/− mice, which have defects in AM differentiation, lacked Sn expression and had reduced GBS clearance following infection. The presence of Siglec-E but absence of Sn in newborn AMs appeared to promote tolerance to GBS. Newborn SigE−/− mice had increased GBS phagocytosis and killing compared to WT controls. We therefore conclude that GBS exploits developmental immaturity of Siglec expression in AMs via its sialic acid capsule in causing neonatal disease.
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9

Chen, Guoyun, Yin wu, and Dongren Ren. "Siglec-E negatively regulates the activation of Toll-like Receptor 4 by controlling its endocytosis." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 222.22. http://dx.doi.org/10.4049/jimmunol.198.supp.222.22.

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Анотація:
Abstract TLR4 signaling is critical for providing effective immune protection but must be tightly controlled to avoid inflammation-induced pathology. Previously, we reported extensive and direct interactions between TLR and Siglec families of Pattern Recognition Receptors. Here, we examined the biological significance of this interaction during infection. We found that Siglec-E is required for E. coli-induced endocytosis of TLR4. Siglec-E-deficient dendritic cells infected with E. coli fail to internalize TLR4. This leads to sustained TLR4 on cell surface and activation of NF-κB and MAP kinase p38, resulting in high levels of TNF-α and IL-6 compared with wild-type dendritic cells. In contrast to the signaling events occurring at the plasma membrane, as a result of the inability to internalize of TLR4, Siglec-E-deficient dendritic cells were also defective for TRIF-mediated IFN-β production in response to E. coli infection. Furthermore, we found that accumulation of ubiquitinated-TLR4 and binding of E3 ubiquitin ligase Triad3A to TLR4 was increased significantly in bone marrow-derived dendritic cells from wild-type mice, but not from Siglec-E-deficient mice, after E. coli infection. This represents a newly discovered mechanism that regulates the signaling of TLR4 during E. coli infection.
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10

Chen, Yin, David J. Friedman, Mayank Saraswat, Michael J. Shapiro, Drew Wilfahrt, Akhilesh Pandey, and Virginia Smith Shapiro. "Sialylation of CD44 by ST8sia6 is required for recognition by the inhibitory receptor Siglec-7." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 176.13. http://dx.doi.org/10.4049/jimmunol.208.supp.176.13.

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Анотація:
Abstract Glycans decorate almost all proteins and lipids on the cell surface, and they play a critical role in cell-cell interactions. Terminal sialic acid addition to glycans helps the immune system distinguish between “self” and “non-self.” The enzyme ST8sia6 adds alpha-2,8 disialic acids to cell surface receptors, and this sialic acid addition promotes binding to the inhibitory receptor Siglec-E. We have previously shown ST8sia6 overexpression in tumors accelerates tumor growth in a Siglec-E dependent manner. Proteomic analysis in murine tumor lines identified CD44 as a target for ST8sia6. CD44 expression on tumors is associated with metastasis and chemoresistance. Since humans and mice have different sialic acid structures, we examined whether ST8sia6 makes CD44 a ligand to the ortholog of Siglec-E in human cells, Siglec-7. When HEK293T cells overexpress ST8sia6 and CD44 together, Siglec-7 binding was significantly increased compared to ST8sia6 or CD44 overexpression alone. Thus, ST8sia6 has a conserved role from mouse to human in decorating CD44 with sialic acid. Our study proposes that ST8sia6 sialylation of CD44 could suppress immune responses and enables cancer progression in human. Supported by grant: 2T32AI007425-23 to DJF and R01 CA243545-01S1 to V.S.S.
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Більше джерел

Дисертації з теми "Siglec-E"

1

Claude, Janine [Verfasser]. "The implication of microglial sialic acid-binding immunoglobulin-like lectin-E (Siglec-E) in neuroinflammation / Janine Claude." Bonn : Universitäts- und Landesbibliothek Bonn, 2014. http://d-nb.info/1049984579/34.

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2

Heins, Anja [Verfasser], and Iris [Akademischer Betreuer] Bruchhaus. "Charakterisierung der immunmodulatorischen Funktion von Siglec-E (Sialinsäure-bindendes-Ig-ähnliches-Lektin-E) im Modell der experimentellen Chagas-Krankheit / Anja Heins. Betreuer: Iris Bruchhaus." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2013. http://d-nb.info/1031756744/34.

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3

Tsai, Ho-Yang, та 蔡和仰. "The role of α2, 8-diSialyl motif in humoral immunity and its interaction with Siglec-E". Thesis, 2017. http://ndltd.ncl.edu.tw/handle/3jy57g.

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Анотація:
碩士
國立臺灣大學
免疫學研究所
105
The role of increasing α2, 8-diSialyl motif synthesized by ST8Sia VI on differentiating B cell surface was unclear. Additionally, it is reported that there is only Siglec-E that can recognize α2, 8-diSialyl motif. We have previously established B cell specific ST8Sia VI knockout (cKO) mice. Our preliminary results showed that ST8Sia VI cKO mice produced higher levels of IgM after immunization. Therefore, in this thesis, we focused on which subsets of B cells contributed to function of α2, 8-diSialyl motif and whether the interplay of Siglec-E was involved. First, we generated that Rbpj and ST8Sia VI B cell-specific double knockout mice, which featured marginal zone B (mzB) cells and α2, 8-diSialyl motif deficiency. These mice showed higher IgM production at the levels similar to those produced by ST8Sia VI cKO mice upon TI antigen immunization. Furthermore, sorted follicle B (foB) cells and B1 cells, but not mzB cells, from ST8Sia VI cKO mice showed stronger activation after stimulation with either LPS or anti-IgM. We also generated SS-KO mice, whose ST8Sia VI and Siglece were deleted, to determine the interaction of Siglec-E and α2, 8-diSialyl motif. We found that SS-KO mice still produced higher amounts of antigen specific IgM than wild type (WT) mice did upon NP-Ficoll immunization, but that the levels of antigen specific IgM in SS-KO mice were similar to that in WT mice after NP-LPS immunization. These results suggested that the interaction between α2, 8-diSialyl motif and Siglec-E may be involved in TLR4 signaling. Furthermore, we found that the higher activation of foB cells from ST8Sia VI cKO mice were compromised after co-cultured with macrophages or neutrophils form Siglece KO mice after LPS stimulation. On the other hand, both Siglece KO and ST8Sia VI cKO B1 B cells were activated better after LPS stimulation. In conclusion, α2, 8-diSialyl motif not only plays an inhibitory role on foB cells but also acts through Siglec-E in both cis- and trans- manners on B1 and foB cells separately.
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4

Kuol, Nyanbol. "Interaction Between Immunosuppressive and Cholinergic Markers in Colorectal Cancer." Thesis, 2020. https://vuir.vu.edu.au/42036/.

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Анотація:
Colorectal cancer (CRC) is amongst the leading diagnosed cancers worldwide. Despite the increasing interest to understand, the roles that the nervous and immune systems play in influencing the tumour microenvironment to promote cancer development and progression, more studies are required to understand the mechanism. Cancer cells can influence their microenvironment and bi-directionally communicate with other systems such as the immune and nervous systems. The immune system plays a key role in the eradication of cancer cells. Studies have shown that multiple mechanisms are responsible for the suppression of the immune system in cancer, one of which being the expression of immune checkpoints inhibitors such as programmed death 1 (PD-1), PD-L1, programmed death ligand 1 and 2 (PD-L1, PD- L2), sialic acid-binding lectins 9 (siglec-9) and IDO (indoleamine-2,3-dioxygenase). These molecules function by inhibiting anti-tumour effects of T cell-mediated immune responses. In addition to these molecules, studies have shown that several cancers can release acetylcholine (ACh) and express cholinergic receptors (muscarinic receptor 3 (M3R) and alpha 7 nicotinic receptor (a7nAChR)), overexpress choline acetyltransferase (ChAT), a precursor enzyme required for ACh synthesis and VAChT, essential for transporting of ACh, and excitatory receptor. Currently, there are no data available in determining the interaction between the expression of immunosuppressive and cholinergic markers in cancer, thus, this thesis aims to determine the interaction between the expression of immunosuppressive and cholinergic markers in CRC.
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5

Erdmann, Hanna [Verfasser]. "Untersuchungen zur Funktion von Siglec-E (sialic acid-binding Ig-like lectin-E) im Verlauf der Trypanosoma-cruzi-(Chagas, 1909)-Infektion in der Maus (Mus musculus, Linnaeus, 1758) / vorgelegt von Hanna Erdmann." 2008. http://d-nb.info/992723337/34.

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6

Marques, Ana Margarida Coelho. "Identificação de Glicanos no estudo do Microambiente Tumoral." Master's thesis, 2018. http://hdl.handle.net/10362/51571.

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7

Soares, Cátia Alexandra Oliveira. "Decoding the molecular recognition of sialic acid-containing glycans by Siglecs." Master's thesis, 2022. http://hdl.handle.net/10362/132001.

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Siglecs are a family of cell surface lectins majorly expressed in immune cells, which through the recognition of sialic acids, present at the terminals of glycans in glycolipids and glycoproteins, modulate immune responses. Hypersialylation is a common phenomenon in cancer cells, which exploits aberrant interactions between cancer-associated sialoglycans and siglecs (namely Siglec-7, -9 and -15) in a strategy to dampen the anti-tumour immune activity. Therefore, understanding the molecular details of the recognition of cancer-associated sialoglycans by siglecs is essential for the development of anticancer therapies. In this work, the molecular recognition of ubiquitous sialoglycans (3’SL and 6’SL) by Siglec-7, -9 and -15, as well the specific recognition of the cancer-associated STn-antigens by Siglec-15, were characterized, using ligand-based Nuclear Magnetic Resonance (NMR) binding experiments such as saturation transfer difference (STD) NMR and tr-NOESY. Overall Siglec-7, -9 and -15 recognize 3’SL and 6’SL similarly. The major determinant for the binding is the Neu5Ac unit, especially its N-acetyl group and glycerol side chain. Subtle differences between siglecs were deduced by STD-derived epitope analysis. Tr-NOESY suggests for 3’SL a conformational selection of the -g conformer (φ=-60°) upon binding. In the case of 6’SL the -g conformer (φ=-60°) is predominant in both free and bound states. Around ω angle, the major conformation in solution is gt but additional studies should be performed to ascertain the conformation in the bound state. Concerning STn antigens (STn-Ser/Thr and STn-PDTRP), the binding towards Siglec-15 is majorly dependent on the Neu5Ac residue, however, GalNAc seems also relevant for the binding. The bioactive conformation around φ dihedral angle for STn-antigens is stabilized around -60° (-g conformer). In the bound state, the determination of ω angle is not conclusive and more studies should be performed. Finally, the effectiveness of the 5G12 antibody in blocking Siglec-15/STn-Ser interactions was also proved by STD-NMR competition experiment.
As siglecs são lectinas expressas nas células do sistema imunitário que modulam respostas imunes através do reconhecimento de ácidos siálicos, presentes nos terminais dos glicanos de glicolípidos e glicoproteínas. A hipersialilação é um fenómeno comum nas células tumorais, que explora a interação com as siglecs (nomeadamente Siglec-7, -9 e -15), como estratégia para diminuir a resposta imunitária anti tumoral. Por isso, entender os determinantes moleculares do reconhecimento de glicanos pelas siglecs é crucial para o desenvolvimento de terapias para o cancro. Neste trabalho caracterizou-se o reconhecimento molecular de ligandos naturais (3’SL e 6’SL) pelas Siglecs-7, -9 e -15, bem como o reconhecimento de antigénios STn associados ao cancro pela Siglec-15, utilizando experiências de Ressonância Magnética Nuclear (STD-RMN e Tr-NOESY). No geral, as Siglecs reconhecem 3’SL e 6’SL de forma semelhante. Dados de STD-RMN indicam que o principal determinante é a unidade Neu5Ac, destacando-se o grupo N-acetilo e a cadeia exocíclica. Diferenças subtis entre as siglecs foram deduzidas através da análise de STD-NMR. No caso da 3’SL, o Tr-NOESY sugere uma seleção conformacional do confórmero -g (φ =-60°) aquando da ligação. Para a 6’SL, o confórmero -g (φ =-60°) é o predominante em ambos os estados livre e complexado. Acerca do ângulo ω, a conformação maioritária em solução é gt (60°), mas estudos adicionais devem ser feitos para determinar a conformação no estado complexado. O reconhecimento dos antigénios STn (STn-Thr/Ser e STn-PDTRP) pela Siglec-15 é maioritariamente dependente do resíduo Neu5Ac, porém o resíduo GalNAc também parece ser relevante na ligação. A conformação bioativa do ângulo φ é maioritariamente -60° (confórmero -g). Quanto ao ângulo ω, os dados no estado complexado não são conclusivos e estudos adicionais são necessários. Por fim, foi demonstrada a eficácia do anticorpo 5G12 no bloqueio da interação Siglec-15/STn-Ser através de uma experiência de competição por STD-NMR.
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Книги з теми "Siglec-E"

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Righini, Enrico. Didisi: Dizionario di sigle, abbreviazioni e simboli. Bologna: Zanichelli, 2001.

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2

Minichiello, Clara. Dizionario di sigle e termini nazionali ed internazionali. Lecce: Pensa multimedia, 1999.

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Minichiello, Clara. Dizionario di sigle e termini nazionali ed internazionali. Lecce: Pensa multimedia, 1999.

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4

Valcárcel, Carmen de Mora. Escritura e identidad criollas: Modalidades discursivas en la prosa hispanoamericana del sigle XVII. Amsterdam: Rodopi, 2001.

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5

Bayle, Françoise. Realizzazioni lessicali sigle e acronimi nei linguaggi settoriali o di specialità in Francia. Fasano (Brindisi): Schena, 2005.

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6

Pasquarelli, Gianni. Le parole dell'economia: Oltre 4000 termini, sigle, citazioni e curiosità per orientarsi nel labirinto del mondo economico. Milano: Pirola, 1993.

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7

Giacomo, Maurizio Di. Opus Dei: La storia, i nomi, le sigle, i collegamenti internazionali, le luci e le ombre della multinazionale di Dio : in appendice, le vecchie e le nuove "Costituzioni" segrete. Napoli: T. Pironti, 1987.

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8

Quartiroli, Ivo. Dizionario acronimi & termini di informatica: Più di 10.000 tra termini, acronimi e sigle, consultazione immediata ed esaustiva, numerosi riferimenti incrociati, più di cento categorie esaurientemente trattate. Milano: Apogeo, 1989.

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9

Cappelli, Adriano. Lexicon abbreviaturarum: Dizionario di abbreviature latine ed italiane usate nelle carte e codici specialmente del Medio-evo riprodotte con oltre 14000 segni incisi : con l'aggiunta di uno studio sulla brachigrafia medioevale, un prontuario di sigle epigrafiche, l'antica numerazione romana ed arabica ed i segni indicanti monete, pesi, misure, etc. 7th ed. Milano: Ulrico Hoepli, 2011.

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10

Andrea, Malossini, ed. Dizionario delle sigle e degli acronimi: [economia, politica, istituzioni, cultura, sport, scienze, tecnologia, informatica, Internet : oltre 8.000 sigle italiane e internazionali, più di 11.000 significati]. Milano: A. Vallardi, 1999.

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Частини книг з теми "Siglec-E"

1

Cuomo, Serafina. "Fibonacci’s Liber Abaci by L. E. Sigler." In Aestimatio: Critical Reviews in the History of Science (Volume 1), edited by Alan C. Bowen and Tracey E. Rihll, 19–27. Piscataway, NJ, USA: Gorgias Press, 2009. http://dx.doi.org/10.31826/9781463221706-005.

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2

D'Amuri, Maria. "Abbreviazioni e sigle." In La casa per tutti nell'Italia giolittiana, 11. Ledizioni, 2013. http://dx.doi.org/10.4000/books.ledizioni.2246.

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3

Urciuoli, Emiliano Rubens. "Abbreviazioni e sigle." In Un’archeologia del “noi” cristiano, 13–18. Ledizioni, 2013. http://dx.doi.org/10.4000/books.ledizioni.2379.

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4

"Sigle e abbreviazioni." In La formazione delle parole in italiano, 645–50. Max Niemeyer Verlag, 2004. http://dx.doi.org/10.1515/9783110934410.645.

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"Abbreviazioni e sigle." In I fiori campestri di Posidippo, 307–10. Göttingen: Vandenhoeck & Ruprecht, 2010. http://dx.doi.org/10.13109/9783666252921.307.

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6

"Sigle e abbreviazioni." In Il corvo bianco, 9–14. Quodlibet, 2022. http://dx.doi.org/10.2307/j.ctv2sbm838.3.

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7

"Sigle e abbreviazioni." In Studi del sesto convegno RBS, 9–12. Peeters Publishers, 2019. http://dx.doi.org/10.2307/j.ctv1q26scv.3.

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8

"SIGLE E ABBREVIAZIONI." In La composizione letteraria del Vangelo di Matteo, 13–16. Peeters Publishers, 2020. http://dx.doi.org/10.2307/j.ctv1q26qfx.3.

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9

"ABBREVIAZIONI E SIGLE." In Gregorio Palamas, Tomo aghioritico, VII—VIII. Peeters Publishers, 2021. http://dx.doi.org/10.2307/j.ctv1q26jp4.3.

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10

"ABBREVIAZIONI E SIGLE." In Il libro del profeta Amos, 27–30. 2nd ed. Peeters Publishers, 2019. http://dx.doi.org/10.2307/j.ctv1q26rnh.4.

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Тези доповідей конференцій з теми "Siglec-E"

1

SABOYA, MELISSA FIUZA, MARIA CLARA DA COSTA FERNANDES, NATÁLIA PONTE FERNANDES, SANDRIELE SANTOS BARBOSA, and TATIANA PASCHOALETTE RODRIGUES BACHUR. "FATORES DE RISCO PARA A CANDIDÍASE VULVOVAGINAL RECORRENTE." In II Congresso Nacional de Microbiologia Clínica On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conamic/07.

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Introdução: A candidíase vulvovaginal recorrente (CVVR) caracteriza-se pela ocorrência de quatro episódios de candidíase vulvovaginal no intervalo de um ano. Essa infecção é causada por fungos do gênero Candida, sendo a espécie C. albicans a mais comum. Objetivo: Realizar um levantamento bibliográfico acerca dos fatores de risco para a ocorrência da CVVR. Métodos: Foi realizada uma pesquisa bibliográfica na base de dados MEDLINE, por meio da utilização dos descritores \"recurrent vulvovaginal candidiasis\" e \"factors\", combinados pelo operador booleano AND. A partir de critérios de inclusão e exclusão pré-estabelecidos, foram selecionados doze artigos para compor este trabalho. Resultados: Existem diferentes fatores que contribuem para o desequilíbrio da microbiota vaginal, levando à proliferação do fungo C. albicans e ao surgimento dos sintomas característicos da CVVR. Os fatores de risco podem ser comportamentais, hormonais, ambientais e genéticos, com a manifestação de polimorfismos em genes específicos. Os genes HLA-DRB1×14, MBL2 e SIGLEC15 estão envolvidos em mutações que ocasionam um menor reconhecimento de epítopos fúngicos e, consequentemente, uma menor resposta imunológica. Quanto aos fatores comportamentais, pode-se citar o uso de roupas apertadas, tecidos sintéticos e absorventes diários, pois ocasionam alterações na umidade e na temperatura na região vulvovaginal. A alimentação rica em carboidratos favorece o crescimento de C. albicans, visto que o glicogênio é o substrato energético do fungo. Em relação aos fatores hormonais, a gravidez, a menopausa e o uso de anticoncepcionais orais resultam em modificações na taxa de progesterona e, consequentemente, numa maior disponibilidade de glicogênio, o que se torna favorável ao crescimento do patógeno. Dentre os fatores ambientais, a utilização de antimicrobianos elimina bactérias comensais da microbiota vaginal, aumentando a disponibilidade de nutrientes para o fungo C. albicans naturalmente residente no local e, consequentemente, facilitando sua proliferação. Além disso, a presença de sêmen pouco viscoso no canal vaginal pode favorecer o crescimento fúngico. Conclusão: A candidíase vulvovaginal recorrente é multifatorial, com importante influência de fatores comportamentais, havendo necessidade de orientações às pacientes acerca das medidas preventivas relacionadas, especialmente, a estes fatores, que são modificáveis.
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Звіти організацій з теми "Siglec-E"

1

DE ANDRADE, RAUL RIBEIRO, OLAVO BARBOSA DE OLIVEIRA NETO, JOÃO GUSTAVO ROCHA PEIXOTO DOS SANTOS, CÉLIO FERNANDO DE SOUSA RODRIGUES, and FABIANO TIMBÓ BARBOSA. Effectiveness of Early Tracheostomy compared with Late Tracheostomy Or Prolonged Orotracheal Intubation in Traumatic Brain Injury: Protocol of Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0051.

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Review question / Objective: What is the effectiveness of Early Tracheostomy compared with Late Tracheostomy Or Prolonged Orotracheal Intubation in Traumatic Brain Injury? Condition being studied: Traumatic Brain Injury (TBI) is every traumatic anatomical ou functional injury that affects brain, skull and/or vessels related to them. TBI is a public health problem that involves over 50 million people per year in Worldwide. Information sources: PUBLISHED DATABASES (Medline by PUBMED, Lilacs, Central-Cochrane, Scopus by Elsevier, Web Of Science e Embase by Elsevier) NON-PUBLISHED (Open Grey by Sigle; Clinical Trial Register at the International Clinical Trials Registry Platform) (Referencies of the selected studies).
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