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Context: Different factors such as the site of infection, the etiological agent, and the immune system can modify the antifungal response of the host. Differences in Sporothrix schenckii strains’ virulence and the host’s immune competency may be involved in the development of sporotrichosis. Nevertheless, the mechanisms related to the disease’s development and progression remain not fully elucidated. Nowadays, no model outweighs the usefulness of mice in biological studies. In these models, transient controlled immunity is created by depressed inflammatory cells during the acute phase of the disease. This is also related to nitric oxide-induced T-cell apoptosis and the lack of a mitogen response. Evidence Acquisition: The recognition of the lipid components of S. schenckii can induce and prolong inflammation. This recognition occurs mainly through the Toll-like receptor (TLR)-4 or the inflammasome. At the same time, TLR-2-mediated identification of fungal exoantigen can serve as an immune evasion process, continuing and worsening the infection. Cell-mediated immune mechanisms have a predominant influence on modulating the clinical expression of sporotrichosis, which is mainly related to Th1/Th17 immunity. Conclusions: In this study, we aimed to explore the innate and acquired immune mechanisms involved in sporotrichosis, as well as the most commonly used animal models for experimental studies.

Sporotrichosis: Review of Innate and Acquired Immune Mechanisms