Autoimmune hepatitis (AIH) is a heterogeneous immune-mediated chronic liver disease affecting children and adults. It is important to rely on a specific animal model to study the hepatic changes and to evaluate the roles played by pro-inflammatory cytokines such as tumor necrosis factor alpha "TNF-α" and transcription factors such as nuclear factor kappa-light-chain-enhancer of activated B cells "NF-κβ" in the pathogenesis and outcome of the disease. This will help to identify specific targets for treatment of AIH.
View Article and Find Full Text PDFβ-Thalassemia (β-thal), is an autosomal recessive disorder caused by mutations at the β gene locus. β-Thalassemia major (β-TM) is a severe form of the disease, characterized by severe hypochromic and hemolytic anemia with an increased need for transfusion. Hemolysis is caused by intoxication, whereas mechanical removal of the affected cells caused by macrophage.
View Article and Find Full Text PDFUnlabelled: Although ultraviolet (UV) radiation is used to treat several types of diseases, including rickets, psoriasis, eczema, and jaundice, the prolonged exposure to its radiation may result in acute and chronic health effects particularly on the skin, eyes, and the immune system.
Aim: This study was carried out to show the effect of UV on both of the lymphoproliferative response and their capacity to produce IL-12 and IL-10 in mice.
Methods: Mice were exposed to whole body UVB and tested for the effect of recovery times on lymphocyte proliferation and cytokine production.
Background: Beta thalassemia is considered a severe, progressive anemia, which needs regular transfusions for life expectancy. One of the most important complications of regular blood transfusions is autoimmunization and alloimmunization, which increases the need for transfusion. This study was performed to investigate the frequency of auto- and allo-antibodies in beta thalassemia patients in Alexandria, Egypt.
View Article and Find Full Text PDFCD55 is a complement regulatory protein expressed by cells to protect them from bystander lysis by complement. It prevents the formation of C3/C5 convertase. In β-thalassemia (β-thal), the defective hemoglobin (Hb) production makes red blood cells (RBCs) lyse early and frequently.
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