Molekulargenetisches Labor
Zentrum für Nephrologie und Stoffwechsel
Die Anfälligkeit für Aspergillose-Infektionen kann genetisch bedingt sein und durch Mutationen in den Genen CLEC1A und CLEC7A hervorgerufen werden.
| 1. |
Seo KW et al. (2005) Protective role of interleukin-10 promoter gene polymorphism in the pathogenesis of invasive pulmonary aspergillosis after allogeneic stem cell transplantation. 
|
| 2. |
Carvalho A et al. (2008) Polymorphisms in toll-like receptor genes and susceptibility to pulmonary aspergillosis.
|
| 3. |
Bochud PY et al. (2008) Toll-like receptor 4 polymorphisms and aspergillosis in stem-cell transplantation.
|
| 4. |
None (2008) TLR polymorphisms and the risk of invasive fungal infections.
|
| 5. |
Levitz SM et al. (2009) Toll-like receptor 4 polymorphisms and aspergillosis.
|
| 6. |
Cervera C et al. (2009) Toll-like receptor 4 polymorphisms and aspergillosis.
|
| 7. |
Asakura Y et al. (2009) Toll-like receptor 4 polymorphisms and aspergillosis.
|
| 8. |
Yokota K et al. (2001) Identification of a human homologue of the dendritic cell-associated C-type lectin-1, dectin-1.
|
| 9. |
Cunha C et al. (2010) Dectin-1 Y238X polymorphism associates with susceptibility to invasive aspergillosis in hematopoietic transplantation through impairment of both recipient- and donor-dependent mechanisms of antifungal immunity.
|
| 10. |
Stappers MHT et al. (2018) Recognition of DHN-melanin by a C-type lectin receptor is required for immunity to Aspergillus.
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