{'fraction_non_alphanumeric': 0.02413793103448276, 'fraction_numerical': 0.0008620689655172414, 'mean_word_length': 4.776119402985074, '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}}
Eosinophil response in mast cell-deficient W/WV mice.

The combination of cyclophosphamide treatment and Toxocara canis infection is known as an effective way of causing a high level of eosinophilia in mice. When this treatment was applied to congenitally anemic, mast cell-deficient W/WV mice, eosinophil response was far less than that of their normal littermate +/+ mice. The degree of the defective eosinophil response in the peripheral blood of W/WV mice was severer than that in the bone marrow. The defective eosinophil response of W/WV mice was completely restored by bone marrow grafting 8 weeks prior to cyclophosphamide treatment and T. canis infection. The kinetics of the recovery of eosinophil response in the bone marrow of W/WV mice after bone marrow grafting was faster than that in the peripheral blood. Chemotactic reactivity of eosinophils obtained from bone marrow or peritoneal cavity of W/WV mice was essentially comparable to that of +/+ mice. These results suggest that, in addition to the production of eosinophils in the bone marrow, mast cell-derived factors play an important role in the mediation of peripheral blood eosinophilia.