Elsevier

Research in Immunology

Volume 149, Issues 4–5, May–June 1998, Pages 321-333
Research in Immunology

Antibody-mediated effects against Cryptococcus neoformans: evidence for interdependency and collaboration between humoral and cellular immunity

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      Among these are included the pro-inflammatory cytokines TNFalpha, IL1beta and IL6 [60] as well as other cytokines that may direct the response primarily towards the Th1 response. It was shown [62] that production of the pro-inflammatory cytokines IL-1beta, IL-2 and TNF-alpha were produced when antibody to GXM was added to human mononuclear cells and C. neoformans. It is believed that immunity to cryptococcosis is based primarily on the cellular system and includes T lymphocytes, NK cells, macrophages and neutrophiles [60].

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      However, in certain conditions, Ab administration to mice with chronic C. neoformans infection can result in catastrophic cardiovascular collapse associated with release of platelet‐activating factor and other proinflammatory mediators (Lendvai et al., 2000; Savoy et al., 1997). Furthermore, experiments with human cells in vitro have clearly demonstrated the same type of antibodies can promote the release of proinflammatory mediators under certain conditions (Vecchiarelli and Casadevall, 1998; Vecchiarelli et al., 1998a,b) (52–54). Consequently, a given Ab can mediate proinflammatory or anti‐inflammatory changes depending on the specific host–microbe interaction.

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      B cells also have an important role in defense. Mouse strains showing a more intense Ab response are more resistant to C. neoformans-induced infection [15]. B-cell-deficient mice (like the CBA/N strain) are more susceptible to infection with the fungus [22].

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