PMC:4503824 / 30343-31724 JSONTXT

{"project":"2_test","denotations":[{"id":"25498576-21699881-43267823","span":{"begin":271,"end":275},"obj":"21699881"},{"id":"25498576-18709538-43267824","span":{"begin":840,"end":844},"obj":"18709538"}],"text":"Eosinophils have been shown to be a major source of Th2 cytokine IL-4 during cryptococcal infection. Eosinophil deficient mice infected with C. neoformans had fewer Th2 cells and increased Th1/Th17 cells, in addition to a reduction of inflammatory cells (Piehler et al., 2011). This again indicates a detrimental role of eosinophils, whereby a Th2 profile is induced in their presence. An interesting clinical observation of an immunocompetent patient with disseminated C. neoformans infection and elevated eosinophil levels, suggests that Cryptococcus is able to induce a Th2 profile that may lead to eosinophilia. However, it was noted that this patient had an atypical Th2 profile, and drugs used for treatment may have increased the eosinophil numbers, and this combination may explain the rarity of this observation (Yamaguchi et al., 2008). The potential capacity of cryptococci to change the host towards a Th2 profile may highlight a mechanism of pathogenicity, with an associated detrimental host response of eosinophil recruitment. Here the differences between the rat and mouse models is intriguing and understanding the molecular differences in their immune response would potentially inform cryptococcal pathogenesis generally, as well as the importance of eosinophilia and a predominant Th2 profile in cryptococcal infection, particularly in HIV infected individuals."}