{'fraction_non_alphanumeric': 0.019681349578256794, 'fraction_numerical': 0.004686035613870665, 'mean_word_length': 5.319526627218935, '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}}
Cytokines Involved in Toxoplasmic encephalitis

Reactivation of cerebral toxoplasmosis occurs in approximately 30% of acquired immune deficiency syndrome (AIDS) patients who are seropositive for Toxoplasma gondii and a change in the levels of cytokines during this relapse is observed. Several cytokines are able to initiate meningeal inflammation and may play a role in the immunopathogenesis of the disease. The induction of a type 1 inflammatory cytokine response is a key event in the initiation of immunity to T. gondii. Interleukin (IL)‐10 production in infected brain facilitates the persistence of parasites by down‐regulating the intracerebral immune response. The in vivo and in vitro models are very numerous and this may explain the heterogeneity of the results. The role of gamma interferon is important because it is the principal mediator inducing a host resistance against T. gondii. Several cytokines stimulating or decreasing interferon (IFN)‐γ levels are reported. The particular case of AIDS patients whose humoral response is altered, is studied.