β-glucan is one of the most abundant cell wall components of fungi. In the early 2000s, dectin 1 was identified as being an innate immune receptor that recognizes β-glucan. Blocking antibodies to dectin 1 abrogated killing of nonopsonized Pneumocystis carinii by alveolar macrophages in vitro and decreased cytokine production in response to pulmonary infection with Aspergillus fumigatus. However, the ultimate proof of a role for dectin 1 in defence against fungi awaited the generation of dectin 1-deficient mice. Two back-to-back publications in 2007 reported opposite results on the role of dectin 1 in clearing systemic Candida albicans infection. Taylor et al. showed that dectin 1-deficient mice (on the 129/Sv background) had reduced inflammatory cell recruitment and increased fungal burden. By contrast, Saijo et al. showed that although dectin 1-deficient mice (on the C57BL/6 background) are more susceptible to P. carinii infection, they are no more susceptible than wild-type mice to C. albicans infection. The mystery of the discrepancy between these results was not solved until 2013 by Marakalala et al.

This study compared the C. albicans strains and the dectin 1-deficient mice that were used by both groups in the 2007 papers. They discovered that the dependency of fungal clearance on dectin 1 is C. albicans strain specific. Surprisingly, dectin 1 dependency is not related to the level of β-glucan exposure. Rather, it correlates with the chitin levels in the cell wall of the fungus. Fungi with high levels of chitin were less dependent on dectin 1 for clearance.

the dependency of fungal clearance on dectin 1 is C. albicans strain specific

These reports had broad implications for the study of fungus–host interactions. Fungal cell wall architecture is complex and adaptable, such that the cell wall architecture of the same fungus may be different in vivo and in vitro. Fungi grown in different culture conditions may differ in their cell wall composition. Fungi having the same name but of different strains may differ in their cell wall composition. In addition, other work has shown that the same cell may use different receptors for different responses to the same fungus. It is not difficult, therefore, to appreciate that the relationship between host and fungus is very complex.