Calcitonin Gene-Related peptide receptor antagonist suppresses allergic asthma responses via downregulation of group 2 innate lymphoid cells in mice

Ike, Erina; Kawano, Tasuku; Takahashi, Katsuro; Miyasaka, Tomomitsu; Takahashi, Tomoko

doi:10.1016/j.intimp.2023.110608

Cited by 4 publications

(2 citation statements)

References 36 publications

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“…Busse WW has high participation in COPD and asthma and found that the IL-33-amphiregulin-osteopontin axis is a potential target for treating fibrosis induced by chronic allergic diseases [ 19 ]. In summary, we found that many influential authors have participated in the study of the relationship between Th2 cells and obstructive pulmonary disease to varying degrees, suggesting the important value of Th2 cells in pulmonary diseases [ 20 , 21 ]. In addition, we listed the top 20 influential authors by Burst detection ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Research trends on airway remodeling: A bibliometrics analysis

Liu,

Wang,

Chen

et al. 2024

Heliyon

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Section: Resultsmentioning

confidence: 99%

Research trends on airway remodeling: A bibliometrics analysis

Liu,

Wang,

Chen

et al. 2024

Heliyon

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“…Activated ILC2s promote the recruitment of eosinophils and initiate a cascade of Th2 responses. These ILC2s can be suppressed upon treatment with CGRP antagonists ( Figure 2C ) ( 90 , 91 ). Targeting ILC2 to inhibit the CGRP signaling is a novel therapeutic strategy for allergy disorders.…”

Section: Role Of Neuropeptides In Neuroimmune Communication In Armentioning

confidence: 99%

Neuroimmune communication in allergic rhinitis

Zhou,

Chen,

Kong

et al. 2023

Front. Neurol.

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The prevalence rate of allergic rhinitis (AR) is high worldwide. The inhalation of allergens induces AR, which is an immunoglobulin E-mediated and type 2 inflammation-driven disease. Recently, the role of neuroimmune communication in AR pathogenesis has piqued the interest of the scientific community. Various neuropeptides, such as substance P (SP), vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP), nerve growth factor (NGF), and neuromedin U (NMU), released via “axon reflexes” or “central sensitization” exert regulatory effects on immune cells to elicit “neurogenic inflammation,” which contributes to nasal hyperresponsiveness (NHR) in AR. Additionally, neuropeptides can be produced in immune cells. The frequent colocalization of immune and neuronal cells at certain anatomical regions promotes the establishment of neuroimmune cell units, such as nerve-mast cells, nerve-type 2 innate lymphoid cells (ILC2s), nerve-eosinophils and nerve-basophils units. Receptors expressed both on immune cells and neurons, such as TRPV1, TRPA1, and Mas-related G protein-coupled receptor X2 (MRGPRX2) mediate AR pathogenesis. This review focused on elucidating the mechanisms underlying neuroimmune communication in AR.

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