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Relevant bibliographies by topics / Cluster Differentiation of Antigen 4

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Journal articles

Academic literature on the topic 'Cluster Differentiation of Antigen 4'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Cluster Differentiation of Antigen 4"

1

Pitcher, Carol, Stefan Höning, Anja Fingerhut, Katherine Bowers, and Mark Marsh. "Cluster of Differentiation Antigen 4 (CD4) Endocytosis and Adaptor Complex Binding Require Activation of the CD4 Endocytosis Signal by Serine Phosphorylation." Molecular Biology of the Cell 10, no. 3 (1999): 677–91. http://dx.doi.org/10.1091/mbc.10.3.677.

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Cluster of differentiation antigen 4 (CD4), the T lymphocyte antigen receptor component and human immunodeficiency virus coreceptor, is down-modulated when cells are activated by antigen or phorbol esters. During down-modulation CD4 dissociates from p56 lck , undergoes endocytosis through clathrin-coated pits, and is then sorted in early endosomes to late endocytic organelles where it is degraded. Previous studies have suggested that phosphorylation and a dileucine sequence are required for down-modulation. Using transfected HeLa cells, in which CD4 endocytosis can be studied in the absence of

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2

La Russa, Raffaele, Aniello Maiese, Rocco Valerio Viola, et al. "Searching for highly sensitive and specific biomarkers for sepsis: State-of-the-art in post-mortem diagnosis of sepsis through immunohistochemical analysis." International Journal of Immunopathology and Pharmacology 33 (January 2019): 205873841985522. http://dx.doi.org/10.1177/2058738419855226.

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The autoptical observations commonly ascribed to sepsis deal with unspecific general and local signs of inflammation or ischemia, such as myocardial inflammation, pulmonary edema and infiltration, cerebral swallowing, and tubular necrosis in the kidney. In the two last decades, some studies have been carried out to implement immunohistochemical markers for post-mortem diagnosis. All of these target molecules are specifically up-regulated or down-regulated during systemic inflammatory responses, especially for infective causes. Among these, we found some antigens expressed on leukocyte surfaces

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3

Rudqvist, Nils, Claire Lhuillier, Maud Charpentier, et al. "465 Radiotherapy and CTLA-4 blockade expand anti-tumor T cells differentiation states and cooperate with CD40 agonist to induce tumor rejection." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A494—A495. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0465.

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BackgroundRadiotherapy (RT) in combination with CTLA-4 inhibition (CTLA4i) can expand and activate T-cells to reject tumors in both mice and some patients with tumors unresponsive to CTLA4i alone.1 2 However, only a subset of patients achieves long-term control of metastatic disease. Similar responses to RT+CTLA4i are seen in the 4T1 mouse model of triple negative breast cancer (TNBC), making it an ideal model to interrogate the interaction between RT and CTLA4i, and identify barriers to its effectiveness.MethodsMice were inoculated in one or both flanks with 4T1 cells. In some experiments one

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4

Peri, Francesco, Valentina Calabrese, Matteo Piazza, and Roberto Cighetti. "Synthetic molecules and functionalized nanoparticles targeting the LPS-TLR4 signaling: A new generation of immunotherapeutics." Pure and Applied Chemistry 84, no. 1 (2011): 97–106. http://dx.doi.org/10.1351/pac-con-11-10-35.

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Toll-like receptor 4 (TLR4), the receptor of bacterial endotoxins in mammalians, plays a pivotal role in the induction of innate immunity and inflammation. TLR4 activation by bacterial lipopolysaccharide (LPS) is achieved by the coordinate and sequential action of three other proteins, the lipopolysaccharide binding protein (LBP), the cluster differentiation antigen CD14, and the myeloid differentiation protein (MD-2) receptors, that bind LPS and present it in a monomeric form to TLR4 by forming the activated [TLR4·MD-2·LPS]2 complex. Small molecules and nanoparticles active in modulating the

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5

Muhammad Rashad, Jaffar Muhammad Baqir, and Ahmed Abdul jabbar Jaloob Aljanaby. "ROLE OF INTERLEUKIN-2, INTERLEUKIN-4 AND CLUSTER OF DIFFERENTIATION-22 AS AN IMMUNE MARKERS IN INDIVIDUALS INFECTED WITH Helicobacter pylori." Journal of Experimental Biology and Agricultural Sciences 9, no. 3 (2021): 388–93. http://dx.doi.org/10.18006/2021.9(3).388.393.

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Helicobacter pylori is a gram-negative, intracellular, microaerophilic bacteria which causing Peptic ulcer. This bacterium can change its shape which helps the bacteria to survive in the host gastric microenvironment. The Peptic ulcer caused by this bacterium stimulates the humoral and cellular immune response in individuals. The current study was carried out to access the role of interleukin-2, interleukin-4, and cluster differentiation-22 as immune markers in the identification of H. pylori infection. The presence of H. pylori has been diagnosed by feces test (antigen rapid test). In this st

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6

Weber, E., D. Schmitter, H. Resch, et al. "Radiation Studies on B Cell Differentiation Marker CD24/SCLC Cluster-4 Antigen Expressing and Non-expressing Lung Cancer Cell Lines and Mouse Fibroblasts." International Journal of Radiation Biology 68, no. 2 (1995): 205–13. http://dx.doi.org/10.1080/09553009514551111.

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7

Lal, Sean, Rodney Lui, Lisa Nguyen, Peter Macdonald, Gareth Denyer, and Cristobal dos Remedios. "Increases in leukocyte cluster of differentiation antigen expression during cardiopulmonary bypass in patients undergoing heart transplantation (vol. 4, Issue 7, pp. 1918-1926)." PROTEOMICS 4, no. 11 (2004): 3660. http://dx.doi.org/10.1002/pmic.200490072.

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8

Solinas, Cinzia, Chunyan Gu-Trantien, and Karen Willard-Gallo. "The rationale behind targeting the ICOS-ICOS ligand costimulatory pathway in cancer immunotherapy." ESMO Open 5, no. 1 (2020): e000544. http://dx.doi.org/10.1136/esmoopen-2019-000544.

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Inducible T cell costimulator (ICOS, cluster of differentiation (CD278)) is an activating costimulatory immune checkpoint expressed on activated T cells. Its ligand, ICOSL is expressed on antigen-presenting cells and somatic cells, including tumour cells in the tumour microenvironment. ICOS and ICOSL expression is linked to the release of soluble factors (cytokines), induced by activation of the immune response. ICOS and ICOSL binding generates various activities among the diversity of T cell subpopulations, including T cell activation and effector functions and when sustained also suppressive

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9

Colden-Stanfield, Margaret. "Clustering of very late antigen-4 integrins modulates K+ currents to alter Ca2+-mediated monocyte function." American Journal of Physiology-Cell Physiology 283, no. 3 (2002): C990—C1000. http://dx.doi.org/10.1152/ajpcell.00481.2001.

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Endothelial cell vascular cell adhesion molecule-1 (VCAM-1) activates adherent monocytes by clustering their very late antigen-4 (VLA-4) receptors, resulting in the modulation of the inwardly rectifying ( I ir) and delayed rectifying ( I dr) K+ currents, hyperpolarization of the cells, and enhanced Ca2+ influx (Colden-Stanfield M and Gallin EK. Am J Physiol Cell Physiol 275: C267–C277, 1998; Colden-Stanfield M and Scanlon M. Am J Physiol Cell Physiol 279: C488–C494, 2000). The present study was undertaken to test the hypothesis that monoclonal antibodies (MAbs) against VLA-4 (MAbVLA-4) mimic V

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10

Harada, Satoshi, Takafumi Segawa, Shigeru Ehara, and Takahiro Sato. "Treatment of primary and metastatic tumors through cancer immunotherapy and abscopal effect by targeted antigen-capturing nanoparticles with programmed death-1 blockade." International Journal of PIXE 28, no. 03n04 (2018): 69–76. http://dx.doi.org/10.1142/s0129083518500158.

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Microcapsules that release antigen-capturing nanoparticles (AC-NPs) with macrophage inflammatory protein-3 alpha (MIP-3[Formula: see text]) and anti-programmed death-1 (PD-1) antibody are developed, and these microcapsules have the ability to enhance immunoresponses through cross-priming of cluster of differentiation 8+ (CD8+) T cells by dendritic cells (DCs) in vivo in BALB/c mice. Lipid protamine hyaluronic acid nanoparticles containing AC-NPs generated via nanoprecipitation of 4 mg/mL of polylactic-co-glycolic acid (PLGA), 1,000 ng/mL of MIP-3[Formula: see text] and 400 [Formula: see text]g

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