A new Anticalin protein for IL-23 inhibits non-type 2 allergen-driven mouse lung inflammation and airway hyperresponsiveness

• Published in: American journal of physiology. Lung cellular and molecular physiology Vol. 327; no. 5; pp. L624 - L633
• Main Authors: Brüggemann, Thayse R, Krishnamoorthy, Nandini, Hagner, Matthias, Matschiner, Gabriele, Jaquin, Thomas, Tavares, Luciana P, Peh, Hong Yong, Levy, Bruce D
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.11.2024
• Subjects: Allergens; Allergens - immunology; Animals; Antibodies, Monoclonal - pharmacology; Asthma; Asthma - immunology; Asthma - metabolism; Asthma - pathology; CD4 antigen; Eosinophils; Female; Helper cells; Inflammation; Interleukin 17; Interleukin 23; Interleukin 5; Interleukin-17 - immunology; Interleukin-17 - metabolism; Interleukin-23 - immunology; Interleukin-23 - metabolism; Leukocytes (eosinophilic); Leukocytes (granulocytic); Leukocytes (neutrophilic); Lung - immunology; Lung - metabolism; Lung - pathology; Lungs; Lymphocytes; Lymphocytes T; Macrophages; Metaplasia; Methacholine; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Monoclonal antibodies; Neutrophils; Neutrophils - immunology; Neutrophils - metabolism; Pneumonia - immunology; Pneumonia - metabolism; Pneumonia - pathology; Proteins; Respiratory Hypersensitivity - immunology; Respiratory Hypersensitivity - pathology; Respiratory tract; Th17 Cells - immunology; Th17 Cells - metabolism; Anticalin proteins; severe asthma; interleukin (IL)-23

Severe asthma is a syndromic label assigned to patients based on clinical parameters, yet there are diverse underlying molecular endotypes in severe asthma pathobiology. Immunophenotyping of asthma biospecimens commonly includes a mixture of granulocytes and lymphocytes. Recently, a subset of patien...