title: Eosinophils express a functional receptor for interferon alpha: inhibitory role of interferon alpha on the release of mediators.
abstract: Recent reports describe the beneficial use of alpha interferon (IFNalpha) for the treatment of idiopathic hypereosinophilic syndrome (HES) unresponsive to conventional therapy. A clinical improvement associated with a rapid decrease of peripheral blood eosinophilia suggested possible direct effects of IFNalpha on eosinophils through the presence of IFNalpha receptors (IFNalphaR). Reverse transcriptase-polymerase chain reaction (RT-PCR) and cytochemistry were used respectively to detect the presence and define the distribution of IFNalphaR on enriched eosinophil preparations purified from blood cells. IFNalphaR was found on eosinophils collected from patients with various eosinophilic disorders. In addition, IFNalpha inhibited the release of eosinophil granule proteins such as eosinophil cationic protein (ECP), neurotoxin (EDN, or interleukin-5 (IL-5). Moreover, antiparasite cytotoxicity was also strongly reduced in a dose-dependent manner by IFNalpha. These results provide the first evidence that human eosinophils express a functional receptor for IFNalpha and represent a potential basis for the beneficial effects of IFNalpha in patients with hypereosinophilic syndromes.
authors.affiliation: Centre d'Immunologie et de Biologie Parasitaire, Unité INSERM U167, Institut Pasteur, Lille, France.
authors.forename: D
authors.initials: D
authors.lastname: Aldebert
authors.forename: B
authors.initials: B
authors.lastname: Lamkhioued
authors.forename: C
authors.initials: C
authors.lastname: Desaint
authors.forename: A S
authors.initials: AS
authors.lastname: Gounni
authors.forename: M
authors.initials: M
authors.lastname: Goldman
authors.forename: A
authors.initials: A
authors.lastname: Capron
authors.forename: L
authors.initials: L
authors.lastname: Prin
authors.forename: M
authors.initials: M
authors.lastname: Capron
mesh_terms: D000818:Animals; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects; D001483:Base Sequence; D001798:Blood Proteins / Q000378:metabolism*; D003594:Cytoplasmic Granules / Q000378:metabolism; D003864:Depression, Chemical; D047091:Eosinophil Granule Proteins; D047208:Eosinophil-Derived Neurotoxin; D004802:Eosinophilia / Q000097:blood*; D004804:Eosinophils / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D017681:Hypereosinophilic Syndrome / Q000097:blood; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000378:metabolism / Q000494:pharmacology*; D015848:Interleukin-5 / Q000378:metabolism*; D008969:Molecular Sequence Data; D009498:Neurotoxins / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D053633:Receptor, Interferon alpha-beta; D017471:Receptors, Interferon / Q000378:metabolism*; D011994:Recombinant Proteins; D012260:Ribonucleases; D012550:Schistosoma mansoni; D012636:Secretory Rate / Q000187:drug effects
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D015848:Interleukin-5; D009498:Neurotoxins; D017471:Receptors, Interferon; D011994:Recombinant Proteins; D053633:Receptor, Interferon alpha-beta; D047208:Eosinophil-Derived Neurotoxin; D012260:Ribonucleases