Publications by authors named "Amjad Mustafa"

Background: Prenatal exposure to the persistent environmental pollutant and model Ah receptor agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has been shown to permanently suppress postnatal cell-mediated immunity. More recently, skewing of select adult T and B cell responses toward enhanced inflammation has also been described in C57BL/6 mice after prenatal TCDD. This raises questions about adverse postnatal immune consequences of prenatal TCDD in animals genetically predisposed to inappropriate inflammatory responses.

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Two immunologically different mouse strains, C57BL/6 and SNF(1), were exposed to a mid-gestation dose of TCDD. The C57BL/6 mouse has a high-affinity aryl hydrocarbon receptor (AhR) and is sensitive to TCDD. The SNF(1) mouse has a low-affinity AhR but spontaneously develops autoimmune nephritis.

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Female SNF(1) hybrid mice spontaneously develop an immune complex-mediated glomerulonephritis as early as 24 weeks of age, whereas the disease onset in males is much slower. Further, a rise in concentration of glomerulus-specific autoantibodies via autoreactive B cells is critical to progression of the disease in this strain. Environmental factors contributing to the onset or degree of such autoimmunity are of interest yet poorly understood.

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Background: Untreated, more than 95% of female SWR x NZB: F(1) (SNF(1)) mice spontaneously develop a fatal lupus-like glomerulonephritis by 8 months-of-age, while disease onset in males is much slower.

Methods: : Timed-pregnant SNF(1) mice (10 per treatment) were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gestational day (GD) 12 by oral maternal gavage with 0, 40, or 80 microg/kg TCDD.

Results: Offspring of the TCDD-exposed dams showed numerous alterations in T lineage cells at 24 weeks-of-age.

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Pregnant C57BL/6 mice were exposed to 5 microg/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or vehicle by oral gavage between gestation days (GDs) 11 and 13. The thymus, spleen, and liver of the pups were examined histologically, and cell surface antigen expression was assessed on postnatal days (PNDs) 1, 14, 25, and 46. In addition to the expected decrease in thymic weight on PND 1, TCDD caused an increase in splenic weight on PND 14 and in hepatic weight on PNDs 14 and 25.

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Previous studies from our laboratory demonstrated that CD44 knockout mice exhibit marked decrease in interleukin (IL)-2-induced vascular leak syndrome (VLS), thereby suggesting a role for CD44 in VLS. In the current study, we tested whether treatment with mAbs against CD44 or hyaluronic acid (HA), the ligand for CD44, can abrogate IL-2-induced VLS. Interestingly, administration of HA caused a marked increase in IL-2-induced VLS in the lungs and liver of C57BL/6 mice.

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