{'fraction_non_alphanumeric': 0.024077046548956663, 'fraction_numerical': 0.006420545746388443, 'mean_word_length': 5.632978723404255, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
In vitro effects of gammaglobulin (IgG) on human monocyte Fc receptor function. I. Effect on monocyte membrane‐associated IgG and Fc receptor‐dependent binding of antibody‐coated platelets

Intravenous immunoglobulin (IV IgG) has been reported to be clinically beneficial for the treatment of immune thrombocytopenic purpura (ITP). The mechanism of effect still remains unknown. We examined the in vitro effects of two commercially available IV IgG preparations. Exposure of normal monocytes to IgG in vitro produced a significant increase in monocyte‐bound IgG. Prior treatment of the commercial IgG preparations by filtration through a 0.2‐μm Millipore filter or ultracentrifugation caused a dramatic decrease in IgG bound to the monocyte surface, indicating that IgG aggregates were responsible for this effect. Exposure of monocytes to IgG levels as high as 150 mg (Sandoglobulin) and 400 mg (Gamimune) did not result in a statistically significant inhibition of monocyte‐platelet interaction as examined by a morphologic rosetting assay. Thus, despite the ability of IV IgG preparations to cause substantial increments in monocyte surface IgG, impairment of Fc receptormediated monocyte binding of antibody‐coated platelets was not observed.