Figure 3
From: Associations of ficolins and mannose-binding lectin with acute myeloid leukaemia in adults
Scheme presenting hypothetical explanation of our results. The G/G homozygosity for the FCN1 gene − 542 G > A polymorphism (related to relatively low ficolin-1 gene expression) and possibly primary MBL deficiency may contribute to impaired clearance of aberrant cells and thus to disease development/progression. That leads to dysregulation of expression of genes encoding for ficolins and MBL, resulting in low ficolin-1 and high ficolin-2, ficolin-3 and MBL (in MBL-sufficient patients) serum concentrations. Aberrant haematopoiesis is associated with impaired immune response to pathogens which is further affected by afore-mentioned dysregulation of production of soluble pattern recognition molecules and chemotherapy (not shown in figure). The protective effect of ficolins and MBL seems to be limited due to impaired phagocytosis (even ficolin- or MBL-opsonized bacterial/fungal cells cannot be eliminated by phagocytes). However, A/A (− 144 C > A, FCN1 gene), C/T and T/T (+ 6,359 C > T, FCN2 gene) genotypes were found to be associated with the most severe infections within short period after chemotherapy).
