Most pathogenic fungi need a stable host-parasite interaction characterized by an immune response strong enough to allow host survival without elimination of the pathogen, thereby establishing commensalisms and latency. Therefore, the balance of pro-inflammatory and anti-inflammatory signaling is a prerequisite for successful host-fungus interaction. In light of these considerations, the responsibilities for virulence is shared by the host and the fungus at the pathogen-host interface, regardless the mode of its generation and maintenance. Studies with C. albicans have provided a paradigm that incorporates contributions from both the fungus and the host to explain the theme of the origin and maintenance of virulence for pathogens and commensals (Romani, 2004a). Through a high degree of flexibility, the model accommodates the concept of virulence as an important component of fungus fitness in vivo within the plasticity of immune responses orchestrated by dendritic cells (DC). Conceptually, this implies that the qualitative development of adaptive response to a fungus may not primarily depend on the nature of the fungal form being presented but rather on the type of cell signaling initiated by the ligand-receptor interaction in DC. Therefore, the functional plasticity of DC at the pathogen-host interface may offer new interpretative clues to fungal virulence.
The host defense mechanisms against fungi are numerous, and range from protective mechanisms that appeared early in the evolution of multicellular organisms (referred to, collectively, as 'innate immunity') to sophisticated adaptive mechanisms, which are specifically induced during infection and disease ('adaptive immunity'). The innate mechanisms appeared early in the evolution of multicellular organisms and act early after the infection. Innate defense strategies are designed to detect broad and conserved patterns which differ between pathogenic organisms and their multicellular hosts. Most of the innate mechanisms are inducible upon infection and their activation requires specific recognition of invariant evolutionarily conserved molecular structures shared by large groups of pathogens by a set of pattern recognition receptors (PRR), including Toll-like receptors (TLR) (Akira & Takeda, 2004). In vertebrates, however, if the infectious organism can breach these early lines of defense an adaptive immune response will ensue, with generation of antigen-specific T helper (Th) effector and B cells that specifically target the pathogen and memory cells that prevent subsequent infection with the same microorganism. The two systems are intimately linked and controlled by sets of molecules and receptors that act to generate a highly coordinated and unitary process for protection against fungal pathogens. The dichotomous Th cell model has proven to be a useful construct that sheds light on the general principle that diverse effector functions are required for eradication of different fungal infections (Romani, 1999). The paradigm has greatly contributed to a better understanding of the host immune response to fungi from a regulatory perspective and has been helpful to accommodate clinical findings in a conceptual framework amenable to strategies of immune-interventions.
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