Source:http://linkedlifedata.com/resource/pubmed/id/16222084
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Predicate | Object |
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rdf:type | |
pubmed:issue |
1
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pubmed:dateCreated |
2005-10-13
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pubmed:abstractText |
CD23, the low-affinity immunoglobulin (Ig)E receptor (FcepsilonRII), is widely distributed on the surface of various human cells. CD23 mediates numerous IgE-related immune responses (including allergen focusing) by enhancing IgE antigen complex presentation, regulating IgE synthesis, influencing cell differentiation and growth of both B- and T-cells, and stimulating production of pro-inflammatory mediators from monocytes/macrophages, eosinophils, and even airway smooth muscle cells. Both membrane and soluble CD23 play an important role in allergic reactions. Cellular contacts and cytokines modulate its expression in a concerted manner as needed for allergic reactions. Expression of CD23 and soluble CD23 has been associated with allergic diseases. Targeting CD23 with monoclonal antibody (MAb) is a promising candidate therapy in allergic diseases. A newly developed agent known as Lumiliximab, which is an anti-CD23 MAb (Lumiliximab), was demonstrated to be a well-tolerated agent in a phase I clinical trial (a placebo-controlled study with allergic asthma). Adverse events were mild, and no relationship was apparent between the dose of Lumilixilab and the frequency, severity, or type of event. Sustained and dose-dependent decreases in mean serum total IgE concentrations were noted. The serum half-life of Lumilixilab increased from 2 to 10 d with increasing doses. Blocking antigen presentation, preventing costimulation signals, and reducing production of pro-inflammatory mediators are some of the potential mechanisms involved for anti-CD23 activity. Although the safety and clinical efficacy of Lumilixilab in allergic asthma and rhinitis require confirmation, the observed data imply that anti-CD23 is a promising candidate therapy option for future treatment of allergic diseases.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1080-0549
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
61-72
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pubmed:dateRevised |
2006-4-27
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pubmed:meshHeading |
pubmed-meshheading:16222084-Animals,
pubmed-meshheading:16222084-Antibodies, Monoclonal,
pubmed-meshheading:16222084-Antigen Presentation,
pubmed-meshheading:16222084-B-Lymphocytes,
pubmed-meshheading:16222084-Cell Differentiation,
pubmed-meshheading:16222084-Humans,
pubmed-meshheading:16222084-Immune Tolerance,
pubmed-meshheading:16222084-Immunoglobulin E,
pubmed-meshheading:16222084-Leukocytes, Mononuclear,
pubmed-meshheading:16222084-Lymphocyte Activation,
pubmed-meshheading:16222084-Receptors, IgE,
pubmed-meshheading:16222084-Respiratory Hypersensitivity,
pubmed-meshheading:16222084-T-Lymphocytes
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pubmed:year |
2005
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pubmed:articleTitle |
Anti-CD23.
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pubmed:affiliation |
Division of Allergy and Immunology, Department of Medicine, National Jewish Medical and Research Center/University of Colorado Health Sciences Center, Denver, CO, USA. rosenwasserl@njc.org
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pubmed:publicationType |
Journal Article,
Review
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