Pregled bibliografske jedinice broj: 109068
IL-18 synergizes IL-12 in inducing B cells to produce interferon-gamma
IL-18 synergizes IL-12 in inducing B cells to produce interferon-gamma // Abstract book
Zagreb, Hrvatska, 2001. str. 2-2 (predavanje, domaća recenzija, sažetak, znanstveni)
CROSBI ID: 109068 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
IL-18 synergizes IL-12 in inducing B cells to produce interferon-gamma
Autori
Servis, Dražen ; Toellner, K.M. ; Grafton, G. ; Branica, Srećko ; Gordon, John ; Gagro, Alenka
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Abstract book
/ - , 2001, 2-2
Skup
2001 Annual Meeting of the Croatian Immunological Society
Mjesto i datum
Zagreb, Hrvatska, 07.12.2001
Vrsta sudjelovanja
Predavanje
Vrsta recenzije
Domaća recenzija
Sažetak
IL-18 has been described as a costimulatory factor to IL-12 for interferon (IFN)-gamma production in T cells, SAC-activated B cells and NK cells. IL-18 mediates its effects by binding to its receptor, IL-18 receptor (IL-18R). Here we ask what impact IL-18, alone or with IL-12, has on the phenotype of B cells engaged in signaling via BCR and CD40, key components in the initiation of T cell-dependent B cell responses. As IL-12 actions on B cells are dependent upon endogenous production of IFN-gamma, we also determined the influence of IL-18 on IFN-gamma expression. To confirm that B cells are responsive to IL-18 we also determined whether B cells express IL-18R on their surface. We found that, in contrast to IL-12, exogenous IL-18 alone or when added together with IL-12 did not further modulate CD23 expression in either unstimulated or in B cells engaged in signaling via BCR and CD40. Neither of these cytokines had any effect on the expression of CD5. IL-18 alone also failed to reproduce the effect of IL-12 on IFN-gamma expression in activated B cells, but it significantly increased IL-12-stimulated IFN-gamma production. We found that B cells expressed IL-18R only after stimulation through BCR and/or CD40 and that exogenous IL-12 further upregulated IL-18R expression. This IL-12 mediated upregulation of IL-18R resulted from a direct effect of IL-12 on activated B cells and was not mediated by IL-12-induced IFN-gamma production since the addition of exogenous IFN-gamma failed to modulate IL-18R expression. Our results indicate that, during T cell dependent B cell responses, human B cells require stimulation with IL-12 to become responsive to IL-18.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
