1 This encapsulated yeast is also able to persist in healthy hosts, thus causing dormant infections that may later be reactivated under an immunosuppressive disease.2 Cryptococcal infections in rats have been shown to have similarities with human cryptococcosis,
revealing a strong granulomatous response and a low susceptibility to disseminated infections.3 T-cell-mediated immunity is a critical component of protective immunity against infection with C. neoformans. Both CD4+ and CD8+ T cells are required for effective immune pulmonary clearance and prevention of extrapulmonary dissemination.4 The cells recruited during the inflammatory response include neutrophils, eosinophils, Ixazomib nmr monocyte/macrophages (Mφ), dendritic cells and lymphocytes [CD4+ T cells, CD8+ T cells, B cells
and natural killer (NK) cells]. Of these cells, activated Mφ, neutrophils and lymphocytes are all capable of in vitro killing or growth inhibition of C. neoformans.5 Related to this, previous studies in our laboratory have shown that Mφ from infected rats appear to be able to kill C. neoformans, principally by generating nitric oxide (NO).6 Moreover, the Obeticholic Acid order NADPH oxidase system was also found to be very important in the mechanism of C. neoformans killing by rat peritoneal cells, with the superoxide anion, hydrogen peroxide (H2O2) Lepirudin and the hydroxyl radical being involved in this process.7 Eosinophils,
in contrast, are implicated as effector cells in helminthic infections, releasing their many cytoplasmic granules, containing toxic molecules, in response to antigenic stimuli.8 Moreover, they notably contribute to allergic inflammation at airway mucosal sites.9 Recent studies have also demonstrated that eosinophils are able to function as antigen-presenting cells (APCs). The eosinophils express major histocompatibility complex (MHC) class I and class II, and the costimulatory molecules CD28, CD40, CD80 and CD86, suggesting that these cells can directly communicate with T cells to regulate immune responses. In addition, eosinophils also secrete a range of cytokines that are not only proinflammatory, but also function as growth factors, stimulants and chemoattractants [e.g. interleukin (IL)-2, IL-4, IL-5, IL-10, IL-12, IL-16, interferon-γ (IFN-γ) and regulated on activation, normal, T-cell expressed, and secreted (RANTES)] for T cells.10 In this sense, eosinophils were demonstrated to present antigens to primed T cells, thus increasing T-helper 2 (Th2) cytokine production.10–14 Furthermore, antigen-loaded eosinophils migrate into local lymph nodes and localize in the T-cell-rich paracortical zones, where they stimulate the expansion of CD4+ T cells.