{'fraction_non_alphanumeric': 0.029804727646454265, 'fraction_numerical': 0.019527235354573486, 'mean_word_length': 5.671232876712328, '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}}
Two distinct pathways of human macrophage differentiation are mediated by interferon‐γ and interleukin‐10

Forming cellular conjugates with T cells, macrophages can help their targets to mount an immune response or they can destroy the targeted T cell. The two functions are performed by two distinct macrophage subsets that can be distinguished by cell surface marker phenotypes, B7+ CD16− and B7− CD16+. Interferon‐γ (IFN‐γ) induces the former, interleukin‐10 (IL‐10) induces the latter phenotype. The two macrophage differentiation pathways are mutually exclusive; each cytokine inhibits the effect of the other cytokine. The second messenger cAMP enhances the macrophage B7 expression and suppresses the macrophage CD16 expression. However, together with IL‐10, cAMP blocks the generation of both macrophage phenotypes. In the chimpanzee we noted deviations from this differentiation pattern that are suggestive of an enhanced IL‐10 presence in the primate environment.