Figure Legends
Figure 1 . Gene expression patterns in sinonasal tissue from patients undergoing surgery in Chicago at Northwestern. Data are from samples from patients with no sinonasal disease (Control, n=11), CRSsNP (9 TunsNP, 5 T1sNP, 8 T2sNP and 5 T3sNP) and CRSwNP (8 ET and 9 NP). The heatmap shows genes with more than 3-fold elevated levels in T1sNP, T2sNP or T3sNP compared to controls. Inspection of the gene expression patterns shows that CRSwNP samples from ethmoid and from nasal polyps are closely aligned with the T2 patterns seen in ethmoid tissue from a subset of patients with CRSsNP. The figure was adapted from published studies by Klingler al 55. Tun – untypeable, T1 – Type 1 endotype, T2 – Type 2 endotype and T3 – Type 3/17 endotype (see text). ET – ethmoid tissue, NP – nasal polyp tissue.
Figure 2 . Overview of the primary cytokines driving T1, T2 and T3 endotypes, the source cells producing the primary cytokines and the effector cells that are recruited to the tissue and activated. Classical endotype refers to earlier endotyping based on the presence or absence of eosinophils. The natural pathogenic targets of each immunological endotype are listed at the bottom of the figure.
Figure 3 . Summary of the major biomarker genes whose expression is elevated in the T1, T2 and T3 endotypes of CRS (whether CRSsNP or CRSwNP). Also shown are the “mixed” endotypes, as indicated by T1,3, T1,2 and T2,3. Not shown are T untypeable (Tun), which do not express the biomarker genes or T1,2,3, a rare group of patients that have elevated levels of all three sets of biomarker genes.
Figure 4 . Overview of recent studies linking disease phenotypic signs and symptoms with molecular endotype, showing the changes in prevalence of each phenotype in the indicated endotypes. It is anticipated that future studies will increasingly link phenotypic signs and symptoms with underlying endotype to better define pathogenic mechanisms and indicate appropriate treatment regimens.