Innate and adaptive type 2 immunity in lung allergic inflammation

Abstract

Allergic inflammation is a type 2 immune disorder classically characterized by high levels of immunoglobulin E (IgE) and the development of Th2 cells. Asthma is a pulmonary allergic inflammatory disease resulting in bronchial hyper-reactivity. Atopic asthma is defined by IgE antibody-mediated mast cell degranulation, while in non-atopic asthma there is no allergen-specific IgE and more involvement of innate immune cells, such as basophils, group 2 innate lymphoid cells (ILC2), and eosinophils. Recently, protease allergens were shown to cause asthmatic responses in the absence of Th2 cells, suggesting that an innate cell network (IL-33/TSLP-basophil-ILC2-IL-5/IL-13 axis) can facilitate the sensitization phase of type 2 inflammatory responses. Recent evidence also indicates that in the chronic phase, these innate immune cells directly or indirectly contribute to the adaptive Th2 cell responses. In this review, we discuss the role of Th2 cytokines (IL-4 and IL-13) and innate immune cells (mast cells, basophils, ILC2s, and dendritic cells) in the cross-talk between innate and adaptive inflammatory responses.

Mast cell‐neural interactions contribute to pain and itch

“…They defend against invading foreign organisms and act as central regulators of the immune system by instantly releasing chemical mediators that orchestrate immune defense and by attracting other cellular entities involved in immune defense. As a result, mast cells are a part of the innate and adaptive immune systems . Mast cells are omnipresent in the body and found near externally exposed surfaces such as the epithelial lining of the skin, mucosa of the gastrointestinal tract, meningeal membrane of the CNS, and airways of the lung.…”

Suppressive Effect of a Thioamide-Related Compound SH-2251 on a Murine Allergic Rhinitis Model

“…Recently, the important role of mucosal epithelial cell-derived cytokine such as IL-25 and IL-33 in the induction of type 2 immune diseases has been reported [23,24). Eosinophilic chronic rhinosinusitis (ECRS) was summarized as an entity of intractable chronic sinus inflammation accompanied by the infiltration of numerous activated eosinophils in the paranasal sinus mucosa and/or nasal polyps [25,26].…”

Type 2 innate lymphoid cells in the induction and resolution of tissue inflammation

“…Within hours of receiving alarmin signals, ILC2s induce type 2 inflammation via production of IL‐5 and IL‐13 . In contrast, antigen‐specific effector T cells need several days to respond, as they must be activated by antigen‐presenting DCs in the draining LNs, differentiate into Th2 cells, and migrate to the site of tissue inflammation . Bridging the time until Th2 cells arrive, ILC2 activity goes beyond activation of innate immunity to communication with DCs and effector T cells.…”