30.1 Immunity to Fungi
Mycoses is another term for fungal infections. Fungal infections are as important as other microbial infections but the lack of animal models for mycoses makes it less informed.
Neutrophils and macrophages serve as the outstanding mediators of innate immunity against fungal infections. Neutrophils release lysosomal enzymes and fungicidal substances like reactive oxygen species, which phagocytose fungi to kill them within the cell.
Cell-mediated immunity is effective mechanism of adaptive immunity against fungal infections. It functions by preventing the spread of fungi to other tissues. Certain Fungi also evoke antibody response of protective value.
30.2 Immunity to viruses
Immune responses towards viruses either function by blocking the infection or by getting rid of infected cells. Type I interferons participate in innate immunity while neutralizing antibodies take part in the adaptive immunity.
30.2.1 Innate immunity to viruses
As mentioned above type I interferons inhibit the infection while the killing of infected cells is mediated by Natural killer (NK) cells. Type I interferons prevent viral replication by triggering an “antiviral state”. NK cells are significant in early stages of the infection because in later stages adaptive immune responses progress. NK cells kill the infected cells and also identify infected cells where the virus has shut off class I MHC expression as an evading mechanism from CTLs. The importance of evading mechanism lies in the fact that the liberation of NK cells from a normal state of inhibition occurs only when MHC class I expression is turned out and not active.
30.2.2 Adaptive immunity to viruses
High affinity antibodies produce adaptive immune response against viral infections by preventing virus binding to the host cells, and by CTLs which bring out elimination of infected cells by killing them. CTLs like CD8+ T-cells identify viral peptides by class I MHC molecule. Further virus infected cell is phagocytosed by the antigen presenting cells such as dendritic cells. Dendritic cells process the viral antigen and present it to naïve CD8+ T-cells. Some of the CD8+ T-cells replicate massively to kill the infected cells. In some cases the virus persists in the infected individual without active replication leading to latent infection. CTLs may lead to tissue injury even if the infectious virus is not dangerous to the body.