Modulation of mite antigen‐induced immune responses by lecithin‐bound iodine in peripheral blood lymphocytes from patients with bronchial asthma

1 Dermatophagoides farinae (Df) mite antigen induced IgE synthesis associated with an imbalance of cytokine production in mite‐sensitive patients with bronchial asthma; increased production of interleukin 4 (IL‐4), and decreased production of interferon‐γ (IFN‐γ) was specifically induced in these patients' lymphocytes. 2 Lecithin‐bound iodine (LBI), with which children with bronchial asthma have been successfully treated in the range of 0.5 to 5 μ m , concentrations comparable to LBI blood levels in medicated individuals, modified mite antigen‐induced immune responses, thereby decreasing abnormal lymphocyte functions. 3 In Df antigen‐driven immune responses, inhibition of IgE generation accompanied by suppression of IL‐4 and the recovery of IFN‐γ production was successful when LBI was used in vitro . 4 LBI also acted on normal PBMCs by downregulating the IL‐4‐induced IgE synthesis, phytohaemagglutin (PHA)‐ and phorbol myristate acetate (PMA) plus calcium ionophore (CaI)‐induced IL‐4 secretion, and by upregulating purified protein derivatives (PPD)‐induced IFN‐γ production. Therefore, LBI was capable of inhibiting the IgE and IL‐4 responses and of enhancing IFN‐γ production both from allergen‐stimulated atopic cells and from non‐atopic cells appropriately stimulated. 5 The expression of human histocompatibility leukocyte antigen (HLA), class II antigens and intercellular adhesion molecule 1 (ICAM‐1) on monocytes, crucial molecules for T cell‐monocyte interactions, was not altered by LBI. 6 LBI probably acts as an immunomodulator to ameliorate mite antigen‐induced abnormal cell‐mediated immune responses in patients with bronchial asthma caused by Df antigen thereby leading to improvement of their clinical status.