Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5383_Библиотеки_им_академика_М_И_Перельмана

The interaction between fungal pathogens and the host immune system is a very complex mechanism involving both innate and adaptive immunity. Skin and epi­thelial surfaces are the first barrier against fungi, and, indeed, many fungal infec­tions occur in patients in whom the integrity of the natural barriers is disrupted. Once the skin’s physical barrier is passed, neutrophils, monocytes, macrophages, natural killer (NK) cells, and dendritic cells (DCs) sense the fungal pathogens, and innate and adaptive immune responses are both activated. The constitutive ele­ments of innate immunity reside in the skin and the mucosal epithelial surfaces, where pattern recognition receptors (PRRs) of innate immune cells such as neutro­phils and macrophages detect fungal pathogen‐associated molecular patterns (PAMPs). The fungal CW is the main source of PAMPs recognized by PPRs in mammalian cells. This detection promotes the engulfment of fungal cells and their subsequent degradation within phagosomal compartments [9, 10]. At the same time, adaptive immunity is activated; for example, antigen‐presenting cells like DCs prime T cells by presenting sampled antigens in association with Major Histocompatibility Complex Class II or Class I molecules, leading to the differen­tiation of CD4 fungal antigens and activate adaptive T‐cell immune responses makes them logical cellular targets for the development of fungal vaccination strategies [12]. T‐cell immune responses, in particular Th1/IL12, are considered key for protective immu­nity to fungi, and a dominant Th1 cell response correlates with protective immunity against fungi and effective fungal vaccines[9]. Therefore, to achieve activation of adaptative immune responses, it is necessary to activate pathogen‐detection mech­anism of the innate immune system. Th17 cytokines have been shown to act as effector molecules during the immune response to fungal infections at the mucosal inflammation and seem to play a critical component of the protective host response to fungal infections. However, need to elicit Th17‐driven response appears not to be crucial for developing an antifungal therapeutic. While antibody‐mediated immu­nity has been considered for a long period of time less important in host defense against fungi, the advances in mAb technology have made it possible to elucidate their protective role, consisting of supporting infection clearance via opsonization or direct antifungal activity[13, 14]. Protective mAbs target protein as well as car­bohydrate epitopes of fungi CW[15–17].