Neuroimmune interactions in peripheral tissues

Klose, Christoph S. N.; Veiga-Fernandes, Henrique

doi:10.1002/eji.202048812

Cited by 30 publications

(10 citation statements)

References 157 publications

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“… 28 , 29 , 30 ILC2 and ILC3, in particular, respond to enteric neuropeptides. 31 DCs and ILC3 also support the production of IgA by plasma cells in the Peyer's patches and the mucosa in response to antigen exposure. Secreted IgA is transported into the lumen and neutralizes pathogenic entities, but its lack of complement binding means it does not contribute to cell lysis, tissue damage or inflammation.…”

Section: The Gut Immune System and Immune Homeostasismentioning

confidence: 95%

Neuronal regulation of the gut immune system and neuromodulation for treating inflammatory bowel disease

2021

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Section: The Gut Immune System and Immune Homeostasismentioning

confidence: 95%

Neuronal regulation of the gut immune system and neuromodulation for treating inflammatory bowel disease

2021

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“…This “neuro-immune crosstalk” plays critical roles in tissue homeostasis ( 42 – 44 ). In addition to the intestinal macrophage ( 45 ), T-cell ( 46 , 47 ), and ILC3 ( 48 ), ILC2s have been investigated for neuro-immune crosstalk from the early stages following identification ( 49 , 50 ). ILC2s express receptors for neuropeptides and neurotransmitters, and are regulated through these receptors.…”

Section: Regulation Of Ilc2mentioning

confidence: 99%

Heterogeneity of ILC2s in the Intestine; Homeostasis and Pathology

et al. 2022

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Group 2 innate lymphoid cells (ILC2s) were identified in 2010 as a novel lymphocyte subset lacking antigen receptors, such as T-cell or B-cell receptors. ILC2s induce local immune responses characterized by producing type 2 cytokines and play essential roles for maintaining tissue homeostasis. ILC2s are distributed across various organs, including the intestine where immune cells are continuously exposed to external antigens. Followed by luminal antigen stimulation, intestinal epithelial cells produce alarmins, such as IL-25, IL-33, and thymic stromal lymphopoietin, and activate ILC2s to expand and produce cytokines. In the context of parasite infection, the tuft cell lining in the epithelium has been revealed as a dominant source of intestinal IL-25 and possesses the capability to regulate ILC2 homeostasis. Neuronal systems also regulate ILC2s through neuropeptides and neurotransmitters, and interact with ILC2s bidirectionally, a process termed “neuro-immune crosstalk”. Activated ILC2s produce type 2 cytokines, which contribute to epithelial barrier function, clearance of luminal antigens and tissue repair, while ILC2s are also involved in chronic inflammation and tissue fibrosis. Recent studies have shed light on the contribution of ILC2s to inflammatory bowel diseases, mainly comprising ulcerative colitis and Crohn’s disease, as defined by chronic immune activation and inflammation. Modern single-cell analysis techniques provide a tissue-specific picture of ILC2s and their roles in regulating homeostasis in each organ. Particularly, single-cell analysis helps our understanding of the uniqueness and commonness of ILC2s across tissues and opens the novel research area of ILC2 heterogeneity. ILC2s are classified into different phenotypes depending on tissue and phase of inflammation, mainly inflammatory and natural ILC2 cells. ILC2s can also switch phenotype to ILC1- or ILC3-like subsets. Hence, recent studies have revealed the heterogeneity and plasticity of ILC2, which indicate dynamicity of inflammation and the immune system. In this review, we describe the regulatory mechanisms, function, and pathological roles of ILC2s in the intestine.

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“…According to some studies, NMU, SP, VIP, and CGRP trigger ILC2 proliferation, then Th2 expansion and expression of allergic inflammation cytokines, including IL-5, though, in most cases, CGRP and VIP exert not pro-inflammatory but anti-inflammatory activities [5,13,17,58,59,83]. Through the cholinergic anti-inflammatory pathway, ACh downregulates ILC2 proliferation [2], and NE limits ILC2-associated type 2 inflammation, and counteracts the activating effects of NMU [63].…”

Section: Neuronal-ilc2unitmentioning

confidence: 99%

Neuronal-Immune Cell Units in Allergic Inflammation in the Nose

Klimov

Cherevko

Klimov

et al. 2022

IJMS

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Immune cells and immune-derived molecules, endocrine glands and hormones, the nervous system and neuro molecules form the combined tridirectional neuroimmune network, which plays a significant role in the communication pathways and regulation at the level of the whole organism and local levels, in both healthy persons and patients with allergic rhinitis based on an allergic inflammatory process. This review focuses on a new research paradigm devoted to neuronal-immune cell units, which are involved in allergic inflammation in the nose and neuroimmune control of the nasal mucociliary immunologically active epithelial barrier. The categorization, cellular sources of neurotransmitters and neuropeptides, and their prevalent profiles in constituting allergen tolerance maintenance or its breakdown are discussed. Novel data on the functional structure of the nasal epithelium based on a transcriptomic technology, single-cell RNA-sequencing results, are considered in terms of neuroimmune regulation. Notably, the research of pathogenesis and therapy for atopic allergic diseases, including recently identified local forms, from the viewpoint of the tridirectional interaction of the neuroimmune network and discrete neuronal-immune cell units is at the cutting-edge.

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Neuroimmune interactions in peripheral tissues

Cited by 30 publications

References 157 publications

Neuronal regulation of the gut immune system and neuromodulation for treating inflammatory bowel disease

Neuronal regulation of the gut immune system and neuromodulation for treating inflammatory bowel disease

Heterogeneity of ILC2s in the Intestine; Homeostasis and Pathology

Neuronal-Immune Cell Units in Allergic Inflammation in the Nose

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