Nephrotic syndrome (NS) is a renal disease characterized by proteinuria and hypoalbuminemia. In NS patients without any allergic disease, serum IgE and IgG4 levels were selectively increased, and peripheral blood mononuclear cells (MNC) spontaneously produced IgE and IgG4. T cells produced interleukin (IL)-13 spontaneously, and B cells constitutively expressed IL-13 receptors (IL-13R). In addition, T cells stimulated surface IgE-negative (sIgE-) and sIgG4- B cells to produce IgE and IgG4, respectively, and IgE and IgG4 production was specifically blocked by anti-IL-13 antibody (Ab). MNC from atopic dermatitis (AD) patients also produced IgE and IgG4 spontaneously. However, in AD patients, T cells spontaneously produced IL-4, but not IL-13, and B cells constitutively expressed IL-4R, but not IL-13R. T cells stimulated sIgE- and sIgG4- B cells to produce IgE and IgG4, respectively, and the production was specifically blocked by anti-IL-4 Ab. On the other hand, sIgE+ and sIgG4+ B cells from both NS and AD patients spontaneously produced IgE and IgG4, respectively, and this production was not affected by T cells, anti-IL-4 Ab, or anti-IL-13 Ab. These results indicate that IL-13 is involved in the enhanced production of IgE and IgG4 in NS, while IL-4 is involved in these responses in AD.

Playing video games enhanced allergic responses with a concomitant increased release of substance P, vasoactive intestinal peptide and nerve growth factor, and skewing of the cytokine pattern toward Th2 type in the patients with atopic eczema/dermatitis syndrome. In addition, exposure to frequently ringing mobile phones also enhanced allergic responses with a concomitant increased release of substance P, vasoactive intestinal peptide and nerve growth factor Collectively, high technology causes stress, which in turn may aggravate symptoms of atopic eczema/dermatitis syndrome.

Objective: The effect of drinking deep-sea water on hair minerals was studied in patients with atopic eczema/dermatitis syndrome (AEDS). Study of hair minerals revealed an imbalance of essential minerals and an increase in toxic minerals in AEDS patients. Design: After drinking deep-sea water (Amami no Mizu) for 6 months in AEDS patients, hair minerals (essential minerals and toxic minerals), clinical evaluation of the skin symptoms were compared before drinking with after drinking. Subjects: After obtaining informed consent, 33 patients (mean age 26 y, range 1-50 y, 13 male and 20 female subjects) with mild to moderate AEDS were enrolled. Results: After drinking deep-sea water, the levels of the essential mineral, potassium (K), were significantly decreased, while the levels of selenium (Se) increased. On the other hand, drinking deep-sea water significantly decreased the levels of the toxic minerals, mercury and lead. Moreover, after drinking deep-sea water, the skin symptoms were improved in 27 out of 33 patients. Conclusion: These results indicate that the mineral abnormalities/imbalance may be involved in the pathogenesis of AEDS, and that drinking deep-sea water may be useful in the treatment of AEDS.

SummaryWe studied the effects of various chemokines including neutrophil-activating peptide 2 (NAP-2), , platelet factor 4 (PF-4), melanoma growth stimulating activity (GRO), ~/interferon-induced protein (IP-10), regulated on activation, normal T expressed and secreted (RANTES), macrophage inflammatory protein lot (MIP-lot), MIP-1 [3, and monocyte chemotactic protein 1 (MCP-1) on Immunoglobulin (IgE) and IgG4 production by human B cells. None of these chemokines with or without interleukin (IL-4), anti-CD40 or -CD58 monoclonal antibody (mAb), induced IgE and IgG4 production by B cells from nonatopic donors. However, RANTES and MIP-lot selectively enhanced IgE and IgG4 production induced by IL-4 plus anti-CD40 or -CD58 mAb without affecting production of IgM, IgG1, IgG2, IgG3, IgA1, or IgA2, whereas other chemokines failed to do so. Enhancement of IgE and IgG4 production by RANTES and MIP-lot was specifically blocked by anti-RANTES mAb and anti-MIP-lot antibody (Ab), respectively, whereas anti-IL-5 mAb, anti-IL-6 mAb, anti-IL-10 Ab, anti-IL-13 Ab, and anti-tumor necrosis factor-6~ mAb failed to do so. Purified surface IgE positive (slgE +) and sIgG4 + B cells generated either in vitro or in vivo spontaneously produced IgE and IgG4, respectively, whereas slgE-and sIgG4-B cells failed to do so. RANTES and MIP-lot enhanced spontaneous IgE and IgG4 production in slgE + and sIgG4 + B cells, respectively, whereas neither RANTES nor MIP-lot did so in sIgE-or slgG4-B cells. Purified sIgE + and sIgG4 +, but not sIgE-or slgG4-B cells, generated in vitro and in vivo expressed receptors for R_ANTES and MIP-lot, whereas they failed to express receptors for other chemokines. These findings indicate that RANTES and MIP-lot enhance IgE and IgG4 production by directly stimulating slgE + and slgG4 + B cells.

SummaryThe effect of interleukin 8 (I1,8) on I1,4-induced immunoglobulin E (IgE) production was studied. I1,4 induced IgE and IgG4 production by tonsiUar mononuclear cells (MNC) without affecting IgM, IgG1, IgA, IgG2, or IgG3 production. IL-8 inhibited I1,4-induced IgE and IgG4 production, whereas it had no effect on IgM, IgG1, IgA, IgG2, and IgG3 production. The inhibitory effect by I1,8 was specific, since it was blocked by anti-I1,8 mAb, but not by control IgG1. Although interferon 3' (IFN-3') also inhibited IgE and IgG4 production by MNC stimulated with I1,4, the inhibitory effect of I1,8 was not mediated by IFN-3', since the I1,8-induced inhibition could not be blocked by anti-IFN-3" mAb. Furthermore, anti-I1,8 mAb had no effect on IFN-3"-induced inhibition. Moreover, addition of I1,5 or I1,6 did not reverse I1,8-induced inhibition of IgE production. In contrast to these observations with MNC, I1,4 failed to induce IgE and IgG4 production by purified B cells. However, combined treatment of purified B cells with I1,4 and anti-CD40 antibody resulted in IgE but not IgG4 production. I1,8 inhibited this IgE production without affecting IgM, IgG1, IgG2, IgG3, IgG4, or IgA production, whereas IFN-3', IFN-c~, or prostaglandin E2 (PGE2) failed to do so. These results indicate that I1,8 antagonizes I1, 4-induced IgE production by directly affecting B cells through a specific mechanism that is different from IFN-3', IFN-o~, or PGE2.