T and B cell activation in childhood allergy : a cross-sectional study of cytokines and immunoglobulins

The newborn immune system differs quantitatively and functionally from that of adults. Development of the immune system has important implications for childhood diseases. The immaturity of the immune system in the first years of life may contribute to failure of tolerance induction and in the development of allergic disease. T-cell function is diminished, especially the capacity to produce cytokines; production of interferon-y (IFN-y) and interleukin-4 (lL-4) is strongly reduced. IFN-y has been found to be even lower in cord blood of newborns with a family history of atopy. Differences in other cell types (natural killer cells, antigen presenting cells and B cells) could also playa role in the development of allergic disease. Current data suggest that irregularities in immunoglobulin E (lgE) synthesis, helper T cell subsets (T h 1, T h2, CD45RA and CD45RO), cytokines (lL-4, IFN-y) and possibly other cell types may playa role in the development of allergy in childhood. Moreover, the role of cell surface molecules, like co-stimulatory molecules (CD2B, CD40L), activation markers (CD25) and adhesion molecules (LFA-1/ICAM-1, VLA-4NCAM-1) is also discussed. These variables are modulated by genetic (relevant loci are identified on chromosome 5q, 11 q and 14) and environmental forces (allergen exposure, viral infections and smoke). The low sensitivity of current predictive factors for the development of allergic diseases, such as cord blood IgE levels, improve in combination with family history and by measurement of in vitro responses of lymphocytes and skin reactivity to allergens. New therapeutic approaches are being considered on the basis of our current understanding of the immunopathology of allergic disease, for instance cytokine therapy and vaccination with tolerizing doses of allergen or peptides.

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