Publication Details
Abstract
The Trichophyton rubrum dermatophytosis is the most common superficial fungal infection in the entire world, which is chronic and recurrent. T. rubrum infection is characterised by a complicated interplay between fungi virulence factors and host cutaneous immunity in their immunopathogenesis. After the invasion of the keratinized tissue, the fungal antigens are detected by the pattern recognition receptors (PRRs), such as Toll-like receptors (TLR2, TLR4) and C-type lectin receptors (Dectin-1) on the keratinocytes, dendritic cells, and macrophages. This awareness triggers intracellular signaling cascades (NF-κB, MAPK pathways), which results in the synthesis of proinflammatory cytokines and chemokines. As active immune sentinels, keratinocytes produce IL-1β, IL-6, TNF-α and antimicrobial peptides that enhance neutrophil and monocyte recruitment to the site of infection. Neutrophils provide the complement to dendritic cells with phagocytosis and reactive oxygen species as well as complement to the T lymphocytes presentation by the dendritic cells. Th1 and Th17 pathways are the most common mediators of adaptive responses. Th1 cells produce IFN- 7 that increases macrophage fungicidal activity, and Th17 cells produce IL-17A, IL-17F, and IL-22 that promote the strengthening of the epithelial barrier and neutrophil recruitment. Nonetheless, T. rubrum is capable of suppressing host immunity through the induction of the anti-inflammatory effects of cytokines like IL-10 to facilitate immune evasion and chronic infection. The persistence, severity and recurrence of any disease is dependent on an imbalance of pro-inflammatory and regulatory cytokines. Host outcomes are further dependent on genetic predisposition, polymorphism of the cytokines, including local skin immune microenvironment. Dynamics Within the framework of T. rubrum dermatophytosis, comprehension of the cytokine networks and cellular immunopathways can be used to inform the design of immunomodulatory treatment solutions and enhance refractory and recurrent infection management strategies