Culture of Plasmodium falciparum in age-fractionated thalassaemic red blood cells (RBC) has shown evidence of parasite damage on light microscopy in older cells during the third culture cycle (96-144 h). In this report, parasites growing in thalassaemic trait and normal RBC were examined ultrastructurally from 96 to 144 h. All parasite stages in old thalassaemic RBC showed evidence of damage worsening with culture duration. There were cytoplasmic alterations with ribosomal damage, and parasite cytoplasm became increasingly loose and grainy, with multiple fissures. Discontinuity of the nuclear membrane with an abnormal nucleolus was seen at l20 h. Cytosomes remained normal, but damage to the food vacuole and shrunken disintegrating parasites were observed at 144 h. These changes are compatible with cellular degeneration and developmental retardation and would account for the schizont maturation arrest and reduced reinvasion rates previously reported. Increased free radicals associated with thalassaemic erythrocytes would explain these changes, further supporting the role for oxidant stress in the protective mechanism.

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Atopic dermatitis is a multifactorial inflammatory skin disease with a complex immunopathogenesis that is characterized by an underlying imbalance of T-cell subsets. Although cytokines of type 2 immunity consistently predominate in the acute phase of atopic dermatitis, there is strong evidence supporting the contribution of cytokines of type 1 immunity, type 3 immunity, and other cytokines in the development and progression of the disease. This review explores the cytokine network in atopic dermatitis, and it highlights areas and causes of controversy in the immunopathogenesis of the disease. In addition, it presents the current therapeutic targets currently being investigated, including monoclonal antibodies and small molecules that inhibit cytokines and downstream signaling molecules in atopic dermatitis. We conclude that atopic dermatitis has a complex and controversial cytokine profile. Understanding the role of cytokines in the immunopathogenesis of the disease is essential for identifying personalized targets for better management and disease control.