Eosinophils are believed to be key effector cells in producing the bronchial mucosal inflammation characteristic of allergic asthma. Given the perceived importance of eosinophils in allergic inflammation, they have been logical therapeutic targets. As knowledge of eosinophil biology increases, eosinophils are targeted with specific therapies blocking their maturation, activation, and chemotaxis. Therapeutic targets include eosinophil-specific cytokines, primarily interleukin-5, and chemokines, eg, eotaxin. Several studies over the last year have reported on therapies effective at reducing eosinophil numbers in asthmatics, including two humanized monoclonal antibodies against interleukin-5 and recombinant human interleukin-12. Surprisingly, despite their effectiveness at depleting eosinophils, there was no evidence of clinical improvement in any of the parameters studied. These and all other relevant studies published within the last year are reviewed by this article. After publication of these studies, some commentators questioned the role of eosinophils in allergic inflammation. Current evidence for and against eosinophils as effector cells in asthma is reviewed.
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http://dx.doi.org/10.1097/00063198-200201000-00006 | DOI Listing |
Front Immunol
January 2025
Central Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.
Background: Uncontrolled severe eosinophilic chronic rhinosinusitis (eCRS) is associated with elevated levels of Th2 cells and raised immunoglobulin concentrations in nasal polyp tissue. eCRS is characterized by high eosinophilic infiltration and type 2 inflammation. Gαi1/3 proteins participate in allergic inflammation by regulating immune cells.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada.
In prednisone-dependent severe asthma, uncontrolled sputum eosinophilia is associated with increased numbers of group 2 innate lymphoid cells (ILC2s). These cells represent a relatively steroid-insensitive source of interleukin-5 (IL-5) and IL-13 and are considered critical drivers of asthma pathology. The abundance of ILC subgroups in severe asthma with neutrophilic or mixed granulocytic (both eosinophilic and neutrophilic) airway inflammation, prone to recurrent infective exacerbations, remains unclear.
View Article and Find Full Text PDFSci Immunol
January 2025
Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.
Thymic stromal lymphopoietin (TSLP) is a type I cytokine that promotes allergic responses and mediates type 2 immunity. A balance between effector T cells (T), which drive the immune response, and regulatory T cells (T), which suppress the response, is required for proper immune homeostasis. Here, we report that TSLP differentially acts on T versus T to balance type 2 immunity.
View Article and Find Full Text PDFSci Rep
January 2025
College of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese Medicine, Nanchang, 330004, China.
Allergic airway inflammation is a universal airway disease induced by inhaling allergens. Published data show that RNF128, an E3 ligase, promotes Th2 activation in the OVA-induced asthma model. Recent advances have shown that group 2 innate lymphoid cells (ILC2s) produce the cytokines IL-5 and IL-13 to mediate type 2 immune response.
View Article and Find Full Text PDFFront Pediatr
December 2024
Department of Pediatrics, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.
Background: () is one of the most common pathogens of community-acquired pneumonia (CAP) in children. Although pneumonia (MPP) is considered a self-limiting disease, severe MPP (SMPP) occurs in some cases. This study aims to analyze clinical features of MPP and to explore predictive indicators in the early stage of infection.
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