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| BIOMARKER | ENDOTYPE | ACTIVATED CYTOKINES | ROLE IN INFLAMMATION PATHWAY | BIOLOGICAL AGENTS |
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| IgE (serum) | T2 high: Allergic | IL-4, IL-13 through activated Th2 cells | Binds FcεRI expressed on the surface of mast cells, eosinophils, basophils and B lymphocytes
Leads to subsequent degranulation and release of mediators | Omalizumab |
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| Eosinophils (serum and sputum) | T2 high: Eosinophilic | IL-5 | Involved in production of reactive oxygen species, desquamation and lysis of airway epithelial cells
Promote airway remodelling | Mepolizumab, Reslizumab, Benralizumab |
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| Surrogate periostin (serum, sputum) | T2 High: Eosinophilic-Allergic | IL-4, IL-13 | Induce an amplification and persistence of chronic inflammation of allergic diseases
Involved in the process of subepithelial fibrosis in asthma patient and in airway remodelling | Lebrikizumab, Tralokizumab, Omalizumab |
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| Exhaled nitric oxide (FeNO) | T2 high: Allergic | IL-4, IL-13 | Useful surrogate of airways inflammation
Due to increased nitric oxide production by activated bronchial epithelial cells | No biological agents, but guideline recommended therapies |
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| Dipeptidyl peptidase 4 (DPP-4 serum) | T2 High: Eosinophilic | IL-13 | Induces the proliferation of airway smooth muscle cells, lung fibroblasts and fibronectin production | Tralokinumab |
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| Galectin-3 (bronchial tissue) | T2 high: Allergic | No target identified | Involved in eosinophil recruitment, airway remodelling and development of Th2 phenotype
Early predictive biomarker of modulation of airway remodelling in severe asthma patients treated with omalizumab. | Omalizumab |
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| Neutrophils (sputum) | T2 low: Neutrophilic/Paucigranulocytic | IL-8 | Induce the release of O2, matrix metalloproteinase-9 (MMP-9), leukotrienes-4 (LTB-4), and platelet-activating factor (PAF) | No biological agents still available |
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