TLR polymorphisms and the risk of invasive fungal infections,” The New England

Allogeneic hematopoietic stem-cell transplantation is a potentially lifesaving cancer therapy that, at least temporarily, renders patients highly immunocompromised and vulnerable to infection. Aspergillus fumigatus, a common environmental fungus that causes invasive infections in immune-compromised persons, is particularly problematic in patients who have undergone this treatment.1 Although the risk of the development of aspergillosis correlates with the degree of immune-suppression and the intensity of exposure to fungal spores, these factors alone do not explain why this infection develops in approximately 5 to 10 % of patients who have received these transplants, whereas it does not develop in the remaining 90 to 95% of patients. A study reported by Bochud and colleagues in this issue of the Journal2 begins to shed light on additional risk factors by correlating innate immune-receptor polymorphisms with the risk of the development of invasive aspergillosis after allogeneic hematopoietic stem-cell transplantation. Innate immune receptors are expressed on or within mammalian cells and, on binding to microbial molecules, induce the expression of factors that restrict microbial tissue invasion and enhance microbial killing.3 The most extensively investigated innate immune receptor