A study of the factors responsible for the development of allergic diseases in early life.

In order to analyze the determinants involved in the development of allergic diseases early in infancy, we examined the environmental and genetic factors that might affect the induction of such diseases during infancy, using a questionnaire. Maternal pharyngitis during pregnancy was significantly related to the development of atopic dermatitis in their progeny. Moreover, the frequency of the maternal infection was associated with a significantly increased risk of allergy in their infants. The prevalence of post-delivery maternal allergy was positively linked to the allergic symptoms in their children while the likelihood of bearing allergic children was related to the numbers of allergic individuals within their family. These results suggested that pre- and post-natal maternal factors and any genetic predisposition might modify the development of allergy in infancy.

Somatropin promotes dermatophagoides farinae-specific IgE generation independently of IL-4 and IL-10.

Interleukin (IL)-10 accelerates the IgE production of anti-CD40- and IL-4-stimulated PBMC by enhancing the IL-6 production of T lymphocytes or antigen-primed spleen cells, in addition to its role as a regulator of the inflammatory responses. To further investigate the mechanisms enhancing IgE synthesis, we determined the effect of somatropin as well as IL-10 on the secretion of Dermatophagoides farinae (Df)-specific IgE by K7 cells, which originate from an EBV-immortalized cell line. Df-pulsed autologous T cells, as well as the supernatants of these cultures, increased the synthesis of Df-specific IgE. Antigen-specific IgE was also enhanced when K7 cells were treated with anti-CD40 antibody and with both IL-4 and IL-10, or with IL-4 and IL-10 without anti-CD40 antibody. The treatment of K7 cells with anti-CD40 antibody and IL-4, or anti-CD40 antibody and IL-10 did not increase IgE production. The Df-specific IgE activity of the supernatants of K7 cells treated with somatropin alone was increased significantly although somatropin did not show any additive effect on the IgE production of anti-CD40 antibody-treated cells. The results indicate that IL-10, a Th2-type cytokine, directly affects the mature B cells that produce IgE, and that the secretion of IgE is increased by treatment with IL-10 in cells that are stimulated with anti-CD40 and IL-4 at the level of the EBV-immortalized cell line, which has already switched to IgE production. Somatropin similarly stimulates activated mature B cells to enhance their production of antigen-specific IgE without class switching, independently of IL-4 and IL-10.