Asthma is the most common chronic disease of childhood in developed countries.1 Recent studies suggest that most asthmatics are diagnosed by the age of five, with symptoms first occurring during infancy and early childhood.2 ,3 Allergy is known to play a significant role in childhood asthma.4-6 The prevalence of allergic diseases including asthma has increased significantly over the past 40 years.7 ,8 The reasons for this increase are not known but are under active investigation. Understanding the pathogenesis of childhood asthma may lead to the development of novel therapies or even to preventive strategies. Little is known about the cellular and molecular mechanisms underlying this disorder. T cells are critical for the initiation and maintenance of the mature asthmatic inflammatory response. Complex interactions between T and B lymphocytes and antigen presenting cells (APC) lead to inflammation, cytokine production, IgE production, and bronchial hyperresponsiveness (BHR). T cell differentiation which will lead to expression of the asthmatic phenotype probably occurs in early childhood under the influence of complex genetic and environmental factors. This review will focus on current knowledge about immune mechanisms of childhood asthma in developed countries. Topics to be discussed include the role of T cells in asthma, maternal-fetal immunological interactions which may promote atopy, the importance of allergens, the antibody response to allergens in early life, T cell function and allergen specific T cell immunity in neonates, cytokine profiles of neonatal lymphocytes, and potential strategies for prevention of childhood asthma.