Blood · 1996 · 87 citations · 20 references
Life SciencesCell BiologyImmunologyInflammationInnate ImmunitySignal TransductionEosinophilic DisordersImmune SignalingInterferon ResponsesIntracellular ReceptorsReceptor RegulationReceptor-mediated SignalingInhibition Of Interferon ResponsesInterferon ProductionInterferon-mediated Innate ImmunityType I Interferon PathwaysType I Interferon Responses
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.
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The idiopathic hypereosinophilic syndrome
IgA-induced eosinophil degranulation.
R I Abu-Ghazaleh, Takao Fujisawa, J Mĕstecký et al. · The Journal of Immunology · 1989 · 387 citations · Full text