Publications by authors named "Hanna Suomalainen"

The precise immune mechanisms behind cow's milk allergy (CMA) are still unknown. Previously, the production of the cytokines TNF-alpha and IFN-gamma in T cells from children with CMA has been shown to be decreased, and the production of IL-4 has been shown to be increased when compared to healthy children. As these aberrations in cytokine production may be associated with disturbances in cellular function, we investigated whether T-cell signal transduction is abnormal in children with CMA.

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Background: The data on lipid metabolism in allergic children is limited.

Objective: We investigated lipid and sterol metabolism in young children whose diets were restricted because of food allergy.

Design: Children in group A [n = 21; mean (+/- SD) age: 1.

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Low interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) production in peripheral blood mononuclear cells (PBMC) from patients with atopic dermatitis and food allergy have been reported previously. However, it remains unclear whether the weak cytokine production is caused by the imbalance of specific T-cell subsets or by dysregulation of T-cell function. In the present study we investigated the intracellular expression of these cytokines at a single-cell level to clarify the background of the disruption.

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The breast-fed infant ingests an average of 108 leucocytes per day, with breast-feeding often continuing for several months. The precise role of human milk leucocytes is still unresolved. Breast-feeding has been recommended for infants at high risk of allergy to prevent or delay the development of food allergies and atopic eczema.

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Introduction: The mechanism for adverse reactions to foods in the gastrointestinal tract are poorly understood. Previous studies of other atopic diseases and animal models suggest that lymphocytes and cytokines may be implicated in the pathogenesis of food allergy.

Aim: The authors investigated the expression of interleukin-4, interferon-gamma and other lymphocyte markers of patients with cereal allergy (wheat, rye, oats) and of controls.

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Objective: To investigate the presence of TRAPS (tumor necrosis factor receptor-associated periodic syndrome), which is a recently defined, dominantly inherited autoinflammatory syndrome caused by mutations in the tumor necrosis factor receptor superfamily 1A gene (TNFRSF1A, CD120a), in a Finnish family with recurrent fever.

Methods: The TNFRSF1A gene was sequenced in both affected and unaffected family members. Flow cytometry and enzyme-linked immunosorbent assay analyses were used to assess membrane expression and serum levels of the TNFRSF1A protein, respectively.

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