Simple understanding and optimistic strategy for coping with atopic diseases. IL-5 central hypothesis on eosinophilic inflammation.
In this article, accumulated investigations were reviewed to present an 'IL-5 central hypothesis' for eosinophilic inflammation. In this simple working hypothesis, mechanisms of clinical amelioration of atopic diseases manifested by glucocorticoids or immunosuppressants such as cyclosporin A or FK506 were easily understood to stem from the inhibition of IL-5 production and gene transcription. Screening of macrolide molecules resulted in the detection of nonactin (code name: OM-01), which inhibits production and gene transcription of IL-5 but not of IL-2 or IL-4. It was suggested that this kind of approach may open a new era of 'specific gene transcription control' for the management of allergic and other human disorders.
Okudaira
H
H
Department of Allergy and Rheumatology, Graduate School of Medicine, University of Tokyo, Japan.
Mori
A
A
D000818:Animals; D004804:Eosinophils / Q000473:pathology*; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000473:pathology* / Q000628:therapy; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D015848:Interleukin-5 / Q000502:physiology*
D015848:Interleukin-5