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Antifungal Immunity

Chaudhary N, Staab JF, Marr KA. PLoS One 2010;5:e9036.

Aspergillus allergens are described as proteins that are recognized in patients with hypersensitivity syndromes such as allergic bronchopulmonary aspergillosis and Aspergillus-induced asthma. However, findings from this study indicate that (at least) some of these proteins are not only allergens, but are also capable of inducing a T-helper 1 (Th1) cytokine response in volunteers without a history of suspected or proven fungal infection or reported allergy or atopy. This indicates that these “Asp f proteins” are able to induce both protective (Th1) and non-protective (Th2) inflammation.

 

Depending on the host’s status, Aspergillus fumigatus is able to cause several diseases ranging from allergic (e.g. Aspergillus-induced asthma and allergic bronchopulmonary aspergillosis) to invasive (e.g. pulmonary aspergillosis and disseminated disease). A fumigatus conidia enter the body via the air and, if they are not cleared by phagocytic cells, spores may germinate. Spore germination leads to the stimulation of macrophages and subsequent production of inflammatory cytokines, which in turn causes dendritic cell (DC) maturation. Once germinated, the fungus induces hyphal growth, which is recognized by neutrophils, resulting in a DC-induced T-lymphocyte response. The T-lymphocyte response can be either protective (T-helper 1 cell [Th1] and Th17 phenotypes) or pathological (Th2 phenotype).

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