[The immune response to fungal infections]

In mycoses congenital--nonspecific innate as well as acquired immunity (involving neutrophiles, monocytes, macrophages, dendritic cells and lymphocytes) both play important roles in host defence. Th1 lymphocytes release cytokines (IL-2, IL-12, IFN gamma) and stimulate cytotoxic cells and neutrophiles to destroy fungal cells. Th2 lymphocytes, on the other hand, suppress cellular immunity by releasing the cytokines IL-4, IL-6 and IL-10 which counter regulate the secretion of IL-2, IL-12, IFN gamma and depress the activity of macrophages. Cellular mechanisms play essential roles in host responses to fungal infections. Dysfunction of T lymphocytes and a reduction in their number are typically observed in patients with mycotic diseases. There occurs a reduction of both T lymphocyte populations and the T-helper to T-suppressor cell number ratio, and these are of critical importance in explaining the diminished IgA production and enhanced adhesion of fungal cells to the surface of host cells as well as in facilitating the intrusion of fungi throughout the skin and mucous membranes. The specific immunological reaction, associated with the synthesis of antibodies against fungal cell wall or cytoplasmic antigens, is of little significance in protective immunity, but nevertheless has a rather important role to play in diagnosis as well as in supporting phagocytosis by inhibition of fungal cell adherence. In patients with mycoses, typically low blood serum level of the immunoglobulin class G and A and low sIgA in saliva are observed. A detailed understanding the nature and function of the immune system in mycoses is necessary to enable improvements in pharmacotherapy with antifungal antibiotics and chemotherapeutics, as well as to treatments based on immunotherapy and vaccination.