Cytokines as targets for the inhibition of eosinophilic inflammation.
Eosinophilic inflammation is thought to play a central role in the pathogenesis of asthma. The immunoregulatory effects of interleukin (IL)-4, IL-5 and immunoglobulin (Ig)E suggest that these molecules play key roles in the effector function of eosinophils and mast cells. IL-4 regulates the development of CD4+ TH2-type cells, which elicit essential signals through IL-4 and IL-5 for the regulation of IgE production and eosinophilia, respectively. IL-5-regulated pulmonary eosinophilia and airways dysfunction can also occur independently of IL-4 and allergen-specific Igs. Such IL-4-independent pathways may also play a substantive role in the aetiology of asthma. Thus, evidence is now emerging that allergic airways disease is regulated by humoral and cell-mediated components. The essential and specific role of IL-5 in regulating eosinophilia, and the subsequent involvement of this leukocyte in the induction of lung damage and airways dysfunction, identifies IL-5 as a primary therapeutic target for the relief of airways dysfunction in asthma.
Hogan
S P
SP
Cellular Signal Transduction Laboratory, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
Foster
P S
PS
D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000628:therapy; D004804:Eosinophils / Q000502:physiology; D006801:Humans; D015847:Interleukin-4 / Q000502:physiology*; D015848:Interleukin-5 / Q000502:physiology; D011657:Pulmonary Eosinophilia / Q000276:immunology*; D013601:T-Lymphocytes / Q000502:physiology
D015848:Interleukin-5; D015847:Interleukin-4