Human Immunodeficiency Virus Lypodystrophy in Hiv-infected Children Is Associated with High Viral Load and Low Cd4 -lymphocyte Count and Cd4 - Lymphocyte Percentage at Baseline and Use of Protease Inhibitors and Stavudne

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platelets in the spleen. Conclusions. The authors concluded that IVIG inhibits autoantibody-mediated thrombocytopenia by inducing inhibitory Fc RIIB receptors on macrophages. The balance of inhibitory (Fc RIIB) and activating (Fc RIII) Fc receptors is likely to be a critical factor in the regulation of macrophage phagocytosis. These results suggest that autoantibody-triggered inflammatory diseases could be treated by new medications that inhibit macrophage phagocytosis. Reviewer’s Comments. IVIG is an effective treatment for many diseases caused by autoantibodies, but its utility is limited by high cost, administration by prolonged intravenous infusion, and the occasional occurrence of side effects such as aseptic meningitis and renal insufficiency. This work suggests that new approaches could be developed that would utilize the same protective mechanism as IVIG, but be more easily administered and potentially have fewer side effects. This research also suggests that defects in the Fc RIIB inhibitory mechanism could underlie antibody-mediated autoimmunity. Although additional work is needed to determine whether the findings in this mouse model apply to human disease, these results are cause for optimism.

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Human Immunodeficiency Virus Lypodystrophy in Hiv-infected Children Is Associated with High Viral Load and Low Cd4 -lymphocyte Count and Cd4 - Lymphocyte Percentage at Baseline and Use of Protease Inhibitors and Stavudne

platelets in the spleen. Conclusions. The authors concluded that IVIG inhibits autoantibody-mediated thrombocytopenia by inducing inhibitory Fc RIIB receptors on macrophages. The balance of inhibitory (Fc RIIB) and activating (Fc RIII) Fc receptors is likely to be a critical factor in the regulation of macrophage phagocytosis. These results suggest that autoantibody-triggered inflammatory disea...

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تاریخ انتشار 2002