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Neuronal-Intraepithelial Lymphocyte Interactions at the Intestinal Mucosa
Publication . Soares, Raquel Maia de Carvalhal; Pirzgalska, Roksana; Veiga-Fernandes, Henrique
Intestinal Intraepithelial Lymphocytes (IELs) are located at the critical interface between the intestinal lumen and the core of the body. Besides constituting the first line of immune defence at the intestinal mucosa, IELs are also essential regulators of this organ homeostasis.
Growing amount of evidence suggest that the immune cell function can be modulated by signals from the intestinal innervation. Importantly, this neuroimmune communication has been shown to be fundamental for the protection of the intestinal mucosa against pathogens and for maintaining tissue homeostasis.
Our preliminary analysis indicated that IELs possess the machinery to integrate neuron-derived signals, therefore we hypothesized that neuronal cues can modulate the function of IELs. We further showed that specific neuronal signals alter the gene expression profile of IELs. Moreover, we also demonstrated the impact of extrinsic factors, such as diet, in shaping these regulatory responses.
These findings establish a possible new layer of local and systemic homeostatic regulation that can be crucial for health.
Regulation of Type 2 Innate Lymphoid Cells in the adipose tissue
Publication . Malpica, Gonçalo André Barata; Veiga-Fernandes, Henrique; Cardoso, Ana
Innate lymphoid cells (ILCs) are a lymphocyte subset which lack adaptive antigen-specific receptors, being the innate counterparts of T helper lymphocytes. ILCs act early in the immune response by producing effector cytokines in response to tissue-derived inducer cytokines. ILC2s, a subtype of ILCs, produce type 2 cytokines in response to helminthic infection, allergens, and epithelial injury. Besides their role in immune defense, ILC2s also contribute to metabolic homeostasis by maintaining an anti-inflammatory protective environment in the adipose tissue (AT). In obesity, excessive lipid accumulation results in chronic low-grade inflammation, causing a shift in immune cell populations that can lead to a systemic metabolic imbalance, known as metabolic syndrome. ILC2-derived molecules act on immune cells and on adipocytes, limiting obesity-induced inflammation and lipid accumulation, respectively. However, how ILC2s perceive environmental cues and integrate signals to maintain AT homeostasis remains poorly understood.
Here, we hypothesize that neuroimmune interactions can control ILC2 function in the AT downstream from sympathetic nervous system innervation.
Using pharmacological, genetic and imaging approaches, we show that AT ILC2s can integrate neuroregulatory molecules to control AT physiology.
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Fundação para a Ciência e a Tecnologia
Programa de financiamento
9471 - RIDTI
Número da atribuição
PTDC/MED-IMU/28366/2017