The range of regulatory T cell (T(R) cell) types that control immune responses is poorly understood. We describe here a population of T(R) cells that developed in vivo from naive CD4(+)CD25(-) T cells during a T helper type 1 (T(H)1)-polarized response, distinct from CD25(+) T(R) cells. These antigen-specific T(R) cells were induced by CD8alpha(+) DCs, produced both interleukin 10 and interferon-gamma, and potently inhibited the development of airway hyper-reactivity. These T(R) cells expressed the transcription factors Foxp3 and T-bet, indicating that these T(R) cells are related to T(H)1 cells. Thus, adaptive T(R) cells are heterogeneous and comprise T(H)1-like T(R) cells as well as previously described T(H)2-like T(R) cells, which express Foxp3 and are induced during the development of respiratory tolerance by CD8alpha(-) DCs.

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While there is increasing information about the pathogenesis and treatment of chronic spontaneous urticaria (csU) in adults, there is little published information about csU in children. Consequently, most of the recommendations contained in current guidelines for the prevention and treatment of csU in infants and children is based on extrapolation of data obtained in adults. To rectify this, this review points out critical gaps in our knowledge and suggests strategies which may help us to improve our understanding of this condition. How common is csU in children? What do we know about its clinical presentation and the presence of useful biomarkers? What are its common underlying causes? What is the course of csU in children? How does csU affect the everyday life of children? What treatment options are available for children? To answer these questions, two separate types of information are required. The first is information about the prevalence of the condition in the community at large and how csU affects the everyday life of both the child-patient and the parent or carer. Because most csU cases in infants and children do not come to specialists but are treated by general practitioners or by parents using over-the-counter medications, these questions may be answered only by general population surveys or schools programmes. The second is clinical information including family history and disease presentation, the presence of biomarkers and comorbidities, objective measures of severity, frequency and duration of exacerbations, the response to therapy and the time to remission. Targeted questionnaires need to be developed and validated for these investigations. This has already begun in Germany with the establishment of the CU-KID Netzwerk (Email address: cu-kid@charite.de), the aim of which is to identify clinical centres and colleagues who treat children with urticaria and to initiate the information gathering described above.

During days 1-4 of antibiotic treatment patients are at elevated risk for HRPA. HRPA are drug-specific and dependent on cumulative annual exposure. Elucidation of HRPA's immunological mechanisms and development of diagnostic algorithms for clinical use are required.

Corticosteroids constitute the most effective current anti-inflammatory therapy for acute and chronic forms of allergic diseases and asthma. Corticosteroids are highly effective in inhibiting the effector function of Th2 cells, eosinophils, and epithelial cells. However, treatment with corticosteroids may also limit beneficial T cell responses, including respiratory tolerance and the development of regulatory T cells (TReg), which actively suppress inflammation in allergic diseases. To examine this possibility, we investigated the effects of corticosteroid administration on the development of respiratory tolerance. Respiratory exposure to Ag-induced T cell tolerance and prevented the subsequent development of allergen-induced airway hyperreactivity. However, treatment with dexamethasone during the delivery of respiratory Ag prevented tolerance, such that allergen sensitization and severe airway hyperreactivity subsequently occurred. Treatment with dexamethasone during respiratory exposure to allergen eliminated the development of IL-10-secreting dendritic cells, which was required for the induction of IL-10-producing allergen-specific TReg cells. Therefore, because allergen-specific TReg cells normally develop to prevent allergic disease and asthma, our results suggest that treatment with corticosteroids, which limit the development of TReg cells and tolerance to allergens, could enhance subsequent Th2 responses and aggravate the long-term course of allergic diseases and asthma.

We conclude that prednisone is not the cause for increased body fat following transplantation; however, it may contribute to lower spontaneous improvements in exercise capacity possibly by limiting increases in muscle strength. The low exercise capacity in all transplant recipients studied at 1 year suggests a need for exercise training to optimize physical functioning following transplant.

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Allergen-specific regulatory T cells play an important role in controlling the development of allergy and asthma.