Conclusions And Perspectives

In the past decades, the frequency of opportunistic fungal infections has increased (Singh 2001). The increasing number of susceptible hosts, the introduction of newer modalities for HSCT, the evolution of organ transplantation practices, the use of novel immunosuppressive agents, and current antimicrobial prophylactic strategies have likely contributed to the changing epidemiology of invasive mycoses. The therapeutic efficacy of antifungals is limited without the help of host immune reactivity. Various cytokines, including chemokines and growth factors, have proved to be beneficial in experimental and human refractory fungal infections (Roilides et al. 2002; Kullberg et al. 2004). The Th1-Th2 balance itself can be the target of immunotherapy (Puccetti et al. 1995; Koguchi and Kawakami 2002). The inhibition of Th2 cytokines, or the addition of Th1 cytokines, can increase the efficacy of antifungals, such as polyens and azoles, in experimental mycoses (Romani 2001).

The appreciation that activation of the innate immune system initiates, amplifies and drives antigen-specific immune responses together with the identification of discrete cell types, specific receptors and the signaling pathways involved in the activation of innate immunity has provided a multitudo of new targets for exploitation by the developments of adjuvants for vaccines (Deepe 2004). Developments in DC biology are providing opportunities for improved strategies for the prevention and management of fungal diseases in immunocompromised patients. The ultimate challenge will be to design fungal vaccines capable of inducing optimal immune responses by targeting specific receptors on DCs. This will require, however, further studies aimed at elucidating the convergence and divergence of pathways of immune protection elicited in infections or upon vaccination.

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