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In-vitro inhibition of antiplatelet autoantibodies by intravenous immunoglobulins and Rh immunoglobulins.

TLDR
In this study, it was observed that immunoglobulins (i.v.IgG & Rh), and their Fab fragments inhibited the binding of antiplatelet autoantibodies to normal platelets, from 15.8 to 90.8 and 25.7% respectively; whereas, their Fc portion did not show any inhibition.
Abstract
Autoimmune thrombocytopenia (AITP) is caused by autoantibodies to platelet glycoprotein antigens. Intravenous immunoglobulin (i.v.IgG) and Rh immunoglobulin infusions have found great significance in the treatment of AITP patients not responding to corticosteroids and other modes of therapy. In our study, it was observed that immunoglobulins (i.v.IgG & Rh), and their Fab fragments inhibited the binding of antiplatelet autoantibodies to normal platelets, from 15.8 to 90.7% and 25.6 to 90.08% respectively; whereas, their Fc portion did not show any inhibition. The presence of specific anti-idiotypic antibodies to antiplatelet autoantibodies was established by using monoclonal antibodies to Glycoprotein IIb/IIa and Glycoprotein Ib/IX, as the specific idiotype source. The i.v.IgG and Rh immunoglobulin products reacted with the monoclonal antibodies, only through their Fab and not through the Fc portions, thereby confirming its specific anti-idiotype activity.

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Journal ArticleDOI

Therapeutic intravenous immunoglobulins

TL;DR: Three areas of active research are discussed, namely the mechanisms of IVIg action in Idiopathic Thrombocytopenic Purpura (ITP), the effects ofIVIg on activated B lymphocytes and the possible involvement of autoantibodies of IgG isotype (auto-IgG) in the immunomodulatory effects of IVG.
Journal ArticleDOI

Effects of intravenous immunoglobulin on platelet count and antiplatelet antibody disposition in a rat model of immune thrombocytopenia.

TL;DR: Experimental support is provided for a new mechanism of IVIG action in ITP (ie, IVIG-mediated increases in antiplatelet antibody elimination) and it is proposed that the observed increase in 7E3 clearance with IVIG therapy is due to saturation of the FcRn salvage receptor for IgG.
Journal ArticleDOI

IVIg inhibits reticuloendothelial system function and ameliorates murine passive-immune thrombocytopenia independent of anti-idiotype reactivity.

TL;DR: The data suggest that IVIg exerts its rapid effect by inhibiting RES function and that anti–idiotype interactions are not required, indicating that antibodies with anti‐idiotypes activity present in IVIG are not necessary for its effective treatment of PIT.
Journal ArticleDOI

Efficacy of IVIG affinity-purified anti-double-stranded DNA anti-idiotypic antibodies in the treatment of an experimental murine model of systemic lupus erythematosus.

TL;DR: Treatment with concentrated specific anti-dsDNA anti-ID prepared from commercial IVIG is more effective in suppressing the humoral reaction and clinical signs of SLE than native IVIG.
Journal ArticleDOI

Immune pathophysiology of autoimmune thrombocytopenic purpura.

TL;DR: This review focuses on cell-mediated and cytokine abnormalities within AITP, and presents data related to the mechanism of action of anti-D.
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