This study indicates that hydrocortisone (HC) Clin. Invest. 1991. 87:870-877.)

No abstract

The regulation of IgE production in B lymphocytes of patients with atopic dermatitis by interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) was studied. IL-4 stimulated IgE production in vitro in B-cells of healthy donors and of children with atopic dermatitis, but had only a marginal effect on the high basal level of IgE production by lymphocytes from adult patients with atopic dermatitis. The addition of IFN-gamma prevented in all cases the stimulation of IgE synthesis induced by IL-4. The production of IgG and IgM was differently influenced. These results indicate that the in vitro production of IgE by mononuclear cells from adult patients is more resistant to the regulatory effects of IL-4 and IFN-gamma than is that in B cells of children with atopic dermatitis. We propose that a previous in vitro test of the responsiveness of IgE-producing B cells to IFN-gamma may be used to select patients with atopic dermatitis for treatment with IFN-gamma.

No abstract

The development of naive CD4 T cells into type 1 or type 2 Th cells has been extensively analyzed in the mouse. Using neonatal CD4 T lymphocytes as a source of human naive cells, we report that these cells may be induced to differentiate into effector cells producing predominantly Th1 or Th2 cytokines. After 3 days of stimulation with anti-CD3 mAb immobilized on CD32 transfected mouse fibroblasts, followed by 3 days of culture in the presence of IL-2, neonatal cells acquire the phenotypic and functional characteristics of effector cells. Primed cells are enriched in CD45R0hi and CD31- cells, and upon stimulation with PMA+ ionomycin they release significant amounts of IL-2, IFN-gamma, IL-4, IL-5, and IL-10. Addition of exogenous cytokines during the period of activation with anti-CD3 markedly alters the profile of cytokine production by primed cells: 1) IL-2 uniformly enhances Th1 and Th2 cytokine production; 2) IL-4 markedly enhances the release of IL-4, IL-5, and IL-10 and suppresses that of IFN-gamma; 3) IFN-gamma strongly inhibits IL-4 and IL-5 production but slightly enhances IFN-gamma release; 4) IFN-alpha markedly inhibits IL-4 and IL-5 production and increases the production of both IFN-gamma and of IL-10; 5) TGF-beta suppresses IL-4 and IL-5 (and to a lesser extent IL-2) production but has inconsistent effect on IL-10 and IFN-gamma production. These effects of exogenous cytokines are not associated with an alteration of CD31 expression on primed cells.