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thymic tuft cells promote an IL-4-enriched medulla and shape thymocyte development; findings indicate that there is a compartmentalized medullary environment in which differentiation of a minor and highly specialized epithelial subset has a non-redundant role in shaping thymic function
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A microRNA array technique and IL-4 transgenic mice were used to demonstrate that IL-4 dysregulates microRNAs involved in inflammation, angiogenesis, lymphangiogenesis and apoptosis
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Downregulation of macrophage Irs2 by hyperinsulinemia impairs IL-4-indeuced M2a-subtype macrophage activation in obesity.
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Ndfip1 preserves Treg lineage stability and immune homeostasis by preventing the expansion of highly proliferative and metabolically active Treg cells and by preventing pathological secretion of IL-4 from Treg cells
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IL-4/ STAT6 signaling needs to be well adjusted to ensure proper development and function of homing Th2 cells.
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By establishing that IL-4 is posttranslationally regulated by TRX-promoted reduction of a disulfide bond, our findings highlight a novel regulatory mechanism of the type 2 immune response that is specific to IL-4 over IL-13.
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The VEGFR1-mediated signaling suppressed IL-4-induced Arg-1 expression.
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The results obtained in the present study suggest that a signaling pathway mediated by FcRg or the FcRg-Syk axis is commonly required for innate basophil IL-4 responses under conditions mimicking encounters with allergen sources.
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IL-4Delta2 did not compete with IL-4 for IL-4Ralpha binding and did not interfere with the downstream STAT-6 phosphorylation in T cells.
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this study shows that IL4 and IL21 cooperate to induce the high Bcl6 protein level required for germinal center formation
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The complex role of IL-4 in autoimmunity and cholangitis.
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The results demonstrate that IL-4 can restore insulin sensitivity in adipocytes via mechanisms not associated with induced adipogenesis or de novo formation of lipid depots.
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Interleukin 4 (IL-4) signaling prevents Chlamydia trachomatis Infection from Inducing upper genital tract (UGT) pathology.
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In the lung, surfactant protein A (SP-A) enhanced interleukin-4 (IL-4)-dependent macrophage proliferation and activation, accelerating parasite clearance and reducing pulmonary injury after infection with a lung-migrating helminth. In the peritoneal cavity and liver, C1q enhancement of type 2 macrophage activation was required for liver repair after bacterial infection.
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Data, including data from studies using transgenic mice, suggest that over-expression of IL4 (interleukin 4) in thyroid tissue/cells up-regulates expression of Duox1 (dual oxidase 1), Duoxa1 (dual oxidase maturation factor 1), and Slc26a4 (pendrin) in thyroid tissue/cells; expression of Slc5a5 (sodium-iodide symporter) is down-regulated.
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NK cells activated by IL-4 in cooperation with IL-15 exhibit distinctive characteristics with enhanced immunologic cytotoxicity.
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we defined a molecular mechanism for IL-4 downregulation of involucrin in keratinocytes, which may play an important role in the pathogenesis of AD.
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In this study, the effect of continuous IL-4 delivery or bioactive implant coating that constitutively releases a protein inhibitor of CCL2 signaling (7ND) on particle induced osteolysis were studied in the murine continuous femoral intramedullary particle infusion model
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T follicular helper (Tfh) cells arise in tumor-draining lymph nodes where they produce an abundance of IL4. Deletion of IL4-expressing Tfh cells improves antitumor immunity, delays tumor growth, and reduces the generation of immunosuppressive myeloid cells in the lymph nodes.
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Findings suggest that interleukin 4 (IL-4) affects anti-tumor immunity and constitutes an attractive therapeutic target to reduce immune suppression in the tumor microenvironment.