Literature DB >> 10466080

CD69 and regulation of the immune function.

R Marzio1, J Mauël, S Betz-Corradin.   

Abstract

CD69, also known as activation inducer molecule, very early activation antigen, MLR-3 and Leu-23, is a member of the natural killer (NK) cell gene complex family of signal transducing receptors. CD69 is as a type II transmembrane glycoprotein with a C-type lectin binding domain in the extracellular portion of the molecule. CD69 expression is induced in vitro on cells of most hematopoietic lineages, including T and B lymphocytes, NK cells, murine macrophages, neutrophils and eosinophils, while it is constitutively expressed on human monocytes, platelets and epidermal Langerhans cells. Although a specific ligand for CD69 has not been identified, its wide cellular distribution and the induction of intracellular signals upon CD69 crosslinking suggest a role for the receptor in the biology of hematopoietic cells. Moreover, certain results indicate that CD69 may be involved in the pathogenesis of such diseases as rheumatoid arthritis, chronic inflammatory liver diseases, mild asthma, and acquired immunodeficiency syndrome.

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Year:  1999        PMID: 10466080     DOI: 10.3109/08923979909007126

Source DB:  PubMed          Journal:  Immunopharmacol Immunotoxicol        ISSN: 0892-3973            Impact factor:   2.730


  68 in total

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4.  Cell contact-dependent PMN HLA-DR and CD69 membrane expression induced by autologous mono-lymphocytes and cell lines.

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Journal:  Inflammation       Date:  2002-08       Impact factor: 4.092

5.  Computationally identifying novel NF-kappa B-regulated immune genes in the human genome.

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6.  Sputum T lymphocytes in asthma, COPD and healthy subjects have the phenotype of activated intraepithelial T cells (CD69+ CD103+).

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8.  IL-1 beta -converting enzyme (caspase-1) in intestinal inflammation.

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9.  Chronic Fatigue Syndrome: The Current Status and Future Potentials of Emerging Biomarkers.

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10.  A possible role of HSP70 in mediating cardioprotection in patients undergoing CABG.

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