Table 1.
Production and action of cytokines over and under-expressed in chronic rhinosinusitis with nasal polyps.
Cytokines | Production | Action |
---|---|---|
Cytokines over-expressed | ||
IL-4 | Th2 lymphocytes, eosinophils, basophils, natural killers and mast cells | Th2 polarization of naïve CD4 T-cells Activation of B-cells and production of Ig [7,8,9] Recruitment of eosinophils [10] Tissue fibrosis [11] Alteration of the epithelial barrier [12,13] |
IL-13 | Th2 lymphocytes, eosinophils, basophils, natural killers and mast cells | Recruitment of inflammatory cells Differentiation of monocytes into macrophages [14,15] Goblet cell hyperplasia [16] Recruitment of eosinophils [17] Alteration of the epithelial barrier [12] |
IL-5 | Th2 lymphocytes, masts cells and eosinophils | Recruitment and survival of eosinophils [18,19,20,21,22,23] Alteration of the epithelial barrier [24] |
IL-9 | Th2, Th9 lymphocytes and mast cells | Inducing IL-5Rα expression [25] Promoting the anti-apoptotic action of IL-5 in asthmatics [25] Production of proteases by mast cells [26] Release of IgE by B-cells [26] Favorizing a muciparous metaplasia [27] |
TSLP | Epithelial cells | Th2 polarization of naive CD4 T-cells [28,29,30] |
IL-1α | Epithelial cells, fibroblasts, monocytes, macrophages, natural killer cells | Recruitment of eosinophils [31,32] |
IL-1β | Epithelial cells, fibroblasts, monocytes, macrophages, natural killer cells | Attraction of monocytes, eosinophils and memory T-cells [33] Glucocorticoid resistance [34] |
IL-33 | Epithelial cells, fibroblasts, macrophages, dendritic cells | Th2 polarization of naïve CD4 T-cells [35] Limitation of neutrophil recruitment [36] Edema formation [37] Mucus production [38] |
TNF-α | Epithelial cells, T lymphocytes, macrophages | Recruitment of eosinophils [10,39,40] Recruitment of monocytes [41] |
IL-6 | T and B lymphocytes, monocytes, fibroblasts, epithelial and endothelial cells | Recruitment of neutrophils [42] Increased epithelial cell proliferation after damage [43] |
OSM | Th2 lymphocytes, eosinophils, neutrophils, and macrophages | Alteration of the epithelial barrier [44] Antifibrotic action |
IL-17 | Th17 lymphocytes | Recruitment of monocytes and neutrophils [45] |
IL-25 | Epithelial cells, mast cells, T lymphocytes | Th2 polarization of naive CD4 T-cells [46] Production of eosinophils [47] |
IL-22 | Th17, Th22 lymphocytes, natural killer cells, eosinophils, epithelial cells | Initiation of TSLP expression [48] Mucus production [49] |
IL-10 | Th2 lymphocytes, B lymphocytes, macrophages, natural killers, ILC2, mast cells | Reduced pathogen elimination [50] |
IL-32 | T lymphocytes, natural killer, monocytes, dendritic cells, endothelial, epithelial cells and fibroblasts | Production of proinflammatory cytokines [51,52] |
Nonconsensual levels of expression | ||
TGF-β | Treg lymphocytes, macrophages, eosinophils and fibroblasts | Reduced activation of eosinophils and proinflammatory cytokines [53,54] Proliferation of fibroblasts and myofibroblast differentiation [55] Epithelial to mesenchymal transition [56] Edema formation [57] |
Cytokines under-expressed | ||
INF-γ | Th1 lymphocytes, ILC1, B lymphocytes, natural killer cells | Th1 polarization of naive CD4 T-cells [58] Recruitment of eosinophils [59] |
IL-2 | T lymphocytes | Treg polarization of naive CD4 T-cells [60] |