ILC2s: Unraveling the innate immune orchestrators in allergic inflammation

Lu, Hui-Fei; Zhou, Yi-Chi; Luo, Dan-Dan; Yang, Dun-Hui; Wang, Xi-Jia; Cheng, Bao-Hui; Zeng, Xian-Hai

doi:10.1016/j.intimp.2024.111899

Cited by 1 publication

(1 citation statement)

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“…Enhanced allergic phenotypes have been described for AhR -/- mice in different models of AAI ( 47 – 49 ), which is in line with the observations of this study, where allergic AhR -/- mice showed an increased grade of AAI with higher levels of Th2 cytokines, and total and OVA-sIgE, yet AIT reduced these markers to a ‘healthy’ wild-type level demonstrating that immune tolerance towards allergens during AIT is not affected by AhR-deficiency. Interestingly, and in line with other studies ( 49 ), the higher levels of BALF Th2 cytokines in allergic AhR -/- mice do not necessarily correlate with a higher proportion of Th2 cells and, therefore, possibly originate from other cell populations, such as ILC2 ( 50 ), or from a differentially regulated immune response due to the lack of AhR signaling, leading to enhanced Th2-related responses ( 47 ).…”

Section: Discussionsupporting

confidence: 83%

Activation of the aryl hydrocarbon receptor improves allergen-specific immunotherapy of murine allergic airway inflammation: a novel adjuvant option?

Heine,

Alessandrini,

Grosch

et al. 2024

Front. Immunol.

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BackgroundAllergen-specific immunotherapy (AIT) is able to restore immune tolerance to allergens in allergic patients. However, some patients do not or only poorly respond to current treatment protocols. Therefore, there is a need for deeper mechanistic insights and further improvement of treatment strategies. The relevance of the aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor, has been investigated in several inflammatory diseases, including allergic asthma. However, its potential role in AIT still needs to be addressed.MethodsA murine model of AIT in ovalbumin-induced allergic airway inflammation was performed in AhR-deficient (AhR-/-) and wild-type mice. Furthermore, AIT was combined with the application of the high-affinity AhR agonist 10-chloro-7H-benzimidazo[2,1-a]benzo[de]iso-quinolin-7-one (10-Cl-BBQ) as an adjuvant to investigate the effects of AhR activation on therapeutic outcome.ResultsAlthough AhR-/- mice suffer stronger allergic responses than wild-type mice, experimental AIT is comparably effective in both. Nevertheless, combining AIT with the administration of 10-Cl-BBQ improved therapeutic effects by an AhR-dependent mechanism, resulting in decreased cell counts in the bronchoalveolar fluid, decreased pulmonary Th2 and Th17 cell levels, and lower sIgE levels.ConclusionThis study demonstrates that the success of AIT is not dependent on the AhR. However, targeting the AhR during AIT can help to dampen inflammation and improve tolerogenic vaccination. Therefore, AhR ligands might represent promising candidates as immunomodulators to enhance the efficacy of AIT.

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