Regulation of Eosinophil and Group 2 Innate Lymphoid Cell Trafficking in Asthma

Asthma is an inflammatory disease usually characterized by increased Type 2 cytokines and by an infiltration of eosinophils to the airways. While the production of Type 2 cytokines has been associated with TH2 lymphocytes, increasing evidence indicates that group 2 innate lymphoid cells (ILC2) play an important role in the production of the Type 2 cytokines interleukin (IL)-5 and IL-13, which likely amplifies the recruitment of eosinophils from the blood to the airways. In that regard, recent asthma treatments have been focusing on blocking Type 2 cytokines, notably IL-4, IL-5, and IL-13. These treatments mainly result in decreased blood or sputum eosinophil counts as well as decreased asthma symptoms. This supports that therapies blocking eosinophil recruitment and activation are valuable tools in the management of asthma and its severity. Herein, we review the mechanisms involved in eosinophil and ILC2 recruitment to the airways, with an emphasis on eotaxins, other chemokines as well as their receptors. We also discuss the involvement of other chemoattractants, notably the bioactive lipids 5-oxo-eicosatetraenoic acid, prostaglandin D2, and 2-arachidonoyl-glycerol. Given that eosinophil biology differs between human and mice, we also highlight and discuss their responsiveness toward the different eosinophil chemoattractants.

Medienart:

E-Artikel

Erscheinungsjahr:

2017

Erschienen:

2017

Enthalten in:

Zur Gesamtaufnahme - volume:4

Enthalten in:

Frontiers in medicine - 4(2017) vom: 10., Seite 136

Sprache:

Englisch

Beteiligte Personen:

Larose, Marie-Chantal [VerfasserIn]
Archambault, Anne-Sophie [VerfasserIn]
Provost, Véronique [VerfasserIn]
Laviolette, Michel [VerfasserIn]
Flamand, Nicolas [VerfasserIn]

Links:

Volltext

Themen:

2-arachidonoyl-glycerol
Asthma
Chemokine
Eosinophil
Eotaxin
Group 2 innate lymphoid cells
Journal Article

Anmerkungen:

Date Revised 29.09.2020

published: Electronic-eCollection

Citation Status PubMed-not-MEDLINE

doi:

10.3389/fmed.2017.00136

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM275212823