First, measurement of methylation levels is semi-quantitative by its nature, prone to artifacts caused by the amplification process, and thus requires validation by other, non-PCR based, methods. We validated our findings using the Human Methylation 450 k BeadChip and found smaller variation in general methylation. However, differences in the matched pairs of nurses remained significantly similar when the two methods were compared. Furthermore, we observed some cytosine background noise for forward sequencing for some samples in our initial tests. By incorporating 20 bp overhangs, that contained C and G nucleotides, at 59 ends of primers, we were able to improve sequence quality and reduce cytosine background significantly. Accurate primer optimization has also been reported to overcome bias in bisulfite methylation analysis. Second, results from peripheral blood leucocytes may not directly be extrapolated to the human brain. However, stress arguably affects the entire body at many levels and, as previously mentioned, serotonin affects a vast range of other functions in that system. The most commonly used source of DNA in SLC6A4 methylation studies is blood tissue. In these studies, DNA is either extracted from peripheral blood leucocytes or from lymphoblast cell lines. Finally, we also acknowledge the heterogeneity of our sample as whole blood samples contain a mixture of various cells that exist in the blood circulation. Third, our small sample size is limiting in terms of statistical power. The original sample size was significantly higher, but it was important to keep a strict selection criteria to rule out the possible effects of smoking, alcohol consumption and medication. This can be viewed as a strength in this study, compared to many others, as smoking and alcohol consumption have been shown to affect DNA methylation. Additionally, our sample was drawn from a large starting cohort Lapatinib enabling us to design a clear contrast in terms of environmental stress based on the well-known Karasek Model. In conclusion, we found that DNA methylation levels at the promoter CpG upstream of SLC6A4 are significantly lower among female nurses working in a high stress environment compared to female nurses working in a low stress environment. In addition, subjective symptoms of burnout were associated with higher methylation levels when the effect of work stress environment was taken into account. 5-HTTLPR does not interact with work stress and methylation, which emphasizes the notable relationship between methylation and environment in the formation of the individual’s phenotype. Our studies of dectin-1 demonstrated an additional mechanism for fungal recognition by neutrophils. Both complement and dectin-1 can be considered ‘primary pathogen recognition systems’ in that they mediate the direct interaction of pathogens with immune cells and are fundamental to cellular processes such as phagocytosis. Without these systems, responses of other pattern recognition receptors are often impaired. In the mouse, dectin-1 seems to play a role in the recognition of non-opsonized Candida albicans by inflammatory cells and macrophages 2, but appeared redundant in the killing of opsonized yeast. C. albicans is one of the main causes of mycoses worldwide. We showed that complement C3 is important for the control of initial C. albicans burdens, but complement seems dispensable for the induction of inflammatory responses as C3-deficient mice exhibited enhanced inflammatory mediator production during infection.