{'fraction_non_alphanumeric': 0.027515047291487533, 'fraction_numerical': 0.012897678417884782, 'mean_word_length': 5.613636363636363, '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}}
critical for erythroblastic island formation Targeted gene deletion demonstrates that cell adhesion molecule ICAM-4 is

ABSTRACT Erythroid progenitors differentiate in erythroblastic islands, bone marrow niches composed of erythroblasts surrounding a central macrophage. Evidence suggests that within islands adhesive interactions regulate erythropoiesis and apoptosis. We are exploring whether erythroid intercellular adhesion molecule-4 (ICAM-4), an immunoglobulin superfamily member, participates in island formation. Earlier, we identified α V integrins as ICAM-4 counterreceptors. Since macrophages express α V , ICAM-4 potentially mediates island attachments. To test this, we generated ICAM-4 knockout mice and developed quantitative, live cell techniques for harvesting intact islands and for reforming islands in vitro. We observed a 47% decrease in islands reconstituted from ICAM-4 null marrow compared to wild type. We also found a striking decrease in islands formed in vivo in knockout mice. Further, peptides that block ICAM-4/α V adhesion produced a 53-57% decrease in reconstituted islands, strongly suggesting that ICAM-4 binding to macrophage α