Abstract

Allergic inflammation is the result of complex immune mechanisms that depends on cytokines produced by Th2 lymphocytes, which gives these cells a pivotal role in the allergic reaction. When activated by allergen, basophils produce IL-4 and IL-13, cytokines key in the allergic inflammatory response. Antigen activation induces expression of these two cytokines by basophils of only about 5–20% of allergic patients; basophils represent 80% of the IL-4 producing cells. Ionomycine can induce the production of these cytokines by basophils from most individuals, regardless of their clinical status. IL-4 production by basophils peaks at 2 h, whereas IL-13 expression is delayed, suggesting that basophils may be involved both in initiation and amplification of the allergic response. Furthermore, the rapid increase in CD40L expression on peripheral blood basophils suggests that they may be involved in IgE production. The CC chemokines increase the production of IL-4 by basophils, and stimulation with a 40-fold lower concentration of antigen then results in an equivalent level of IL-4 production. Diesel exhaust particles induce early IL-4 production by the majority of basophils, regardless of the individual’s allergic status; this effect is dependent on the generation of reactive oxygen species. Taken as a whole, these data add weight to the conclusion that basophils are involved in the pathophysiology of allergic diseases. In addition to their critical role in allergic inflammation, basophils may also be involved in anti-infectious immunity through the nonspecific mechanisms involved in innate immunity

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