Granulocyte-macrophage colony-stimulating factor modulates tapasin expression in human neutrophils

• Published in: Journal of leukocyte biology Vol. 65; no. 2; pp. 205 - 210
• Main Authors: Ouakfaoui, Souad El, Heitz, Dominique, Paquin, Robert, Beaulieu, André D.
• Format: Journal Article
• Language: English
• Published: United States Society for Leukocyte Biology 01.02.1999
• Subjects: Antiporters - genetics; Antiporters - metabolism; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology; Histocompatibility Antigens Class I - metabolism; HL-60 Cells - drug effects; HL‐60 cells; Humans; Immunoglobulins - genetics; Immunoglobulins - metabolism; Membrane Transport Proteins; MHC class‐I; Neutrophils - drug effects; Neutrophils - metabolism; Polymerase Chain Reaction; RNA, Messenger - metabolism
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1002/jlb.65.2.205

Differential display‐polymerase chain reaction (DD‐PCR) was used to evaluate changes in mRNA expression of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) treated human neutrophils to better understand how this cytokine affects the functions of neutrophils at the molecular level. Although a variety of cDNA fragments were identified as modulated by GM‐CSF with the use of DD‐PCR, one fragment in particular, NGS‐17 (neutrophil GM‐CSF‐stimulated fragment #17), was characterized. The NGS‐17 fragment hybridized to a 3.8‐kb mRNA that encodes for a protein of a predicted molecular mass of 47.6 kDa. After cloning and sequencing, this gene was found to code for the recently sequenced tapasin or TAP‐A protein. Immunoprecipitation and immunoblotting studies using anti‐tapasin antibodies showed that tapasin is expressed in neutrophils and is associated with the MHC class I‐TAP complex. Moreover, tapasin expression was found to be induced by dimethyl sulfoxide and by retinoic acid in HL‐60 cells. This is the first report on the expression of tapasin in human neutrophils. It provides novel information, at the molecular level, on how GM‐CSF enhances the functions of these cells. J. Leukoc. Biol. 65: 205–210; 1999.