Difference between revisions of "Immunity to Fungi"
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| − | Cutaneous and superficial fungal infections are normally self-limiting, with recovery associated with a resistance to re-infection. As hosts often develop delayed-type [[Hypersensitivity - | + | Cutaneous and superficial fungal infections are normally self-limiting, with recovery associated with a resistance to re-infection. As hosts often develop delayed-type [[Hypersensitivity - Introduction|hypersensitivity]], this resistance appears to be cell-mediated. |
*[[T cell differentiation|T cell]] immunity- it is thought that [[T cell differentiation#TH1 Cells|helper T cells]] release cytokines to activate [[Macrophages|macrophages]] to fight the infection | *[[T cell differentiation|T cell]] immunity- it is thought that [[T cell differentiation#TH1 Cells|helper T cells]] release cytokines to activate [[Macrophages|macrophages]] to fight the infection | ||
*[[Neutrophils|Neutrophils]]- there is now growing evidence for the role of [[Neutrophils|neutrophils]] in some infections of the respiratory system, with defensin and the nitric oxide pathways implicated | *[[Neutrophils|Neutrophils]]- there is now growing evidence for the role of [[Neutrophils|neutrophils]] in some infections of the respiratory system, with defensin and the nitric oxide pathways implicated | ||
Latest revision as of 13:23, 18 August 2010
Cutaneous and superficial fungal infections are normally self-limiting, with recovery associated with a resistance to re-infection. As hosts often develop delayed-type hypersensitivity, this resistance appears to be cell-mediated.
- T cell immunity- it is thought that helper T cells release cytokines to activate macrophages to fight the infection
- Neutrophils- there is now growing evidence for the role of neutrophils in some infections of the respiratory system, with defensin and the nitric oxide pathways implicated