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Results suggest that ILT3 played an important role in tumor progression in colorectal cancer by possible influence on CD45RO+ T cells in the tumor microenvironment.
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These results suggest that tyrosine phosphorylation may be critical in FcgammaRI-dependent endocytosis/phagocytosis that may be regulated by LILRB4 by triggering dephosphorylation of key signalling proteins.
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ILT3 may functionally contribute to a regulatory network controlling tumor progression by suppressing the Akt pathway.
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The ILT3 PBs/PCs were suggested to be developmentally equivalent based on the simultaneous generation of these populations upon activation of memory B cells in vitro ILT3 expression was found to be induced efficiently by IL-2, while IFN-alpha effectively induced ILT3 PBs/PCs in vitro Utilizing the elevated ILT3 will support opening a new avenue for molecular markers for, pathogenic cells.
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this study shows that LILRB4 might have dual inhibitory and activating functions, depending on the position of the functional tyrosine residues in its immunoreceptor tyrosine-based inhibitory motifs and/or the nature of the stimuli
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LILRB4 expression is significantly upregulated in human masticatory mucosa during wound healing
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Identification of ILT4 as a cellular receptor for CSP C4d
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involvement of ILT3 and ILT4 in the modulation of immune responsiveness in multiple sclerosis by both interferon and vitamin D
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Cyclosporine up-regulated the expression of ILT3 and ILT4 on natural killer cells, which influenced their cytotoxicity against tumor cells.
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ILT3Fc inhibits T cell activation and induces the generation of suppressor T cells targeting multiple inflammatory miRNA pathways.
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Crystal structure of leukocyte Ig-like receptor LILRB4 (ILT3/LIR-5/CD85k): a myeloid inhibitory receptor involved in immune tolerance.
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upregulated on antigen-presenting cells in response to Salmonella infection
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Data show that LILRB4 is a potent inhibitor of monocyte activation via FcgammaRI.
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report that ILT2 receptor, ILT3 receptor, ILT4 receptor, and KIR2DL4 receptor expression is up-regulated by HLA-G histocompatibility antigen in antigen-presenting cells, natural killer cells, and T cells
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ILT3 precursor RNA is expressed and retained in nuclei of resting endothelial cells.
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Our findings indicate that expression of ILT3 and ILT4 on CLL B cells represents a phenotypic abnormality that may play a role in tolerization of tumor-specific T cells.
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The inhibitory effect of serum and membrane ILT3 in a humanized SCID mouse model describes an immune-escape mechanism that could contribute to impaired T cell responses in patients with cancer.
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Both membrane and soluble ILT3 are proteins with potent immunosuppressive activity which are of importance for treatment of rejection, autoimmunity and cancer.
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describe an immune-escape mechanism mediated by the inhibitory receptor immunoglobulin-like transcript 3 (ILT3) which may be responsible for failure of pancreatic cancer therapy
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Progenitor mast cells expressed cell surface inhibitory LILRB4. Mature cord-blood-derived mast cells had detectable mRNA encoding multiple LILRs, none were expressed on the cell surface.