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Single-Cell Analysis: A Method for In-Depth Phenotyping of Cells Involved in Asthma

Asthma is a chronic inflammatory lung disease with high prevalence, making it one of the most common chronic conditions worldwide. Its pathophysiology is influenced by a range of genetic and environmental factors, resulting in a complex and heterogeneous disease profile. Asthma is primarily associat...

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Bibliographic Details
Published in:International journal of molecular sciences 2024-12, Vol.25 (23), p.12633
Main Authors: Rodríguez-González, Daniel, Guillén-Sánchez, Gema, Del Pozo, Victoria, Cañas, José Antonio
Format: Article
Language:English
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Summary:Asthma is a chronic inflammatory lung disease with high prevalence, making it one of the most common chronic conditions worldwide. Its pathophysiology is influenced by a range of genetic and environmental factors, resulting in a complex and heterogeneous disease profile. Asthma is primarily associated with a type 2 (T2) immune response, though non-T2 endotypes also contribute to disease pathology. Generally, asthma is characterized by the infiltration and activation of various cell types, including dendritic cells, eosinophils, innate lymphoid cells, lymphocytes, mast cells, and neutrophils, which participate in T1, T2, and T17 immune responses. Despite advances in understanding, many questions remain unresolved. Therefore, emerging omic techniques, such as single-cell RNA sequencing (scRNA-seq), offer novel insights into the underlying mechanisms of asthma and the roles of these immune cells. Recent scRNA-seq studies in asthma have identified multiple novel immune cell subtypes and clusters, suggesting their potential functions in disease pathology. The rapid advancement of scRNA-seq technology now enables in-depth investigation of individual cells within tissues, allowing for precise cell-type classification and detailed molecular profiling. Nonetheless, certain limitations persist, which require further refinement in future studies.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms252312633