Innate Lymphocytes in Adipose Tissue Homeostasis and Their Alterations in Obesity and Colorectal Cancer

Cornò, Manuela Del; Conti, Lucia; Gessani, Sandra

doi:10.3389/fimmu.2018.02556

Cited by 16 publications

(15 citation statements)

References 59 publications

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“…Inflammation has been longer considered a key aspect in the pathogenesis of cancer [ 47 ] and compelling evidence has been achieved that an inflammatory state or in turn attenuation of inflammation may favor or prevent cancer development, respectively. Altered immune functions, both systemic and within the AT, have been consistently reported in obese individuals [ 48 , 49 , 50 ] and are thought to represent a main contributor to the obesity-associated greater risk for chronic diseases, including cancer, as well as to the increased prevalence and severity of common infections [ 51 ]. The immune dysfunctions observed under obesity rely on the excess AT and adipocyte hypertrophy that promote proinflammatory cytokines release, both locally and systemically [ 52 ], and excessive recruitment and infiltration of immune cells, especially macrophages [ 53 , 54 ].…”

Section: The Link Between Obesity and Cancermentioning

confidence: 99%

Type I Interferons as Joint Regulators of Tumor Growth and Obesity

Gessani

Belardelli

2021

Cancers

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Type I interferons (IFN-I) are antiviral cytokines endowed with multiple biological actions, including antitumor activity. Studies in mouse models and cancer patients support the concept that endogenous IFN-I play important roles in the control of tumor development and growth as well as in response to several chemotherapy/radiotherapy treatments. While IFN-I signatures in the tumor microenvironment are often considered as biomarkers for a good prognostic response to antitumor therapies, prolonged IFN-I signaling can lead to immune dysfunction, thereby promoting pathogen or tumor persistence, thus revealing the “Janus face” of these cytokines in cancer control, likely depending on timing, tissue microenvironment and cumulative levels of IFN-I signals. Likewise, IFN-I exhibit different and even opposite effects on obesity, a pathologic condition linked to cancer development and growth. As an example, evidence obtained in mouse models shows that localized expression of IFN-I in the adipose tissue results in inhibition of diet–induced obesity, while hyper-production of these cytokines by specialized cells such as plasmacytoid dendritic cells in the same tissue, can induce systemic inflammatory responses leading to obesity. Further studies in mouse models and humans should reveal the mechanisms by which IFN-I can regulate both tumor growth and obesity and to understand the role of factors such as genetic background, diet and microbioma in shaping the production and action of these cytokines under physiological and pathological conditions.

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Section: The Link Between Obesity and Cancermentioning

confidence: 99%

Type I Interferons as Joint Regulators of Tumor Growth and Obesity

Gessani

Belardelli

2021

Cancers

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“…Obesity alters preexisting adipocyte hypertrophy, preadipocyte differentiation, macrophages, T-cell infiltration at the adipose site, the release of inflammatory cytokines, and increases insulin resistance (IR) [ 5 ]. In ATs, cytokines and chemokines are released by both adipocytes and immune cells [ 6 ], and the dysfunction of these AT-derived-cytokines and chemokines may result in hypoxia, and excess secretion of free fatty acids (FFAs) [ 7 ]. Moreover, the infiltration of immune cells and the excessive accumulation of macrophages may also contribute to FFA release [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity

Kiran

Kumar

et al. 2021

Cells

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Obesity is characterized as a complex and multifactorial excess accretion of adipose tissue (AT) accompanied with alterations in the immune response that affects virtually all age and socioeconomic groups around the globe. The abnormal accumulation of AT leads to several metabolic diseases, including nonalcoholic fatty liver disorder (NAFLD), low-grade inflammation, type 2 diabetes mellitus (T2DM), cardiovascular disorders (CVDs), and cancer. AT is an endocrine organ composed of adipocytes and immune cells, including B-Cells, T-cells and macrophages. These immune cells secrete various cytokines and chemokines and crosstalk with adipokines to maintain metabolic homeostasis and low-grade chronic inflammation. A novel form of adipokines, microRNA (miRs), is expressed in many developing peripheral tissues, including ATs, T-cells, and macrophages, and modulates the immune response. miRs are essential for insulin resistance, maintaining the tumor microenvironment, and obesity-associated inflammation (OAI). The abnormal regulation of AT, T-cells, and macrophage miRs may change the function of different organs including the pancreas, heart, liver, and skeletal muscle. Since obesity and inflammation are closely associated, the dysregulated expression of miRs in inflammatory adipocytes, T-cells, and macrophages suggest the importance of miRs in OAI. Therefore, in this review article, we have elaborated the role of miRs as epigenetic regulators affecting adipocyte differentiation, immune response, AT browning, adipogenesis, lipid metabolism, insulin resistance (IR), glucose homeostasis, obesity, and metabolic disorders. Further, we will discuss a set of altered miRs as novel biomarkers for metabolic disease progression and therapeutic targets for obesity.

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“…People with obesity exhibit a general proinflammatory profile. Changes of cytokine/adipokine secretion by adipocytes and free FA release by AT couple with dramatic changes in the immune cell repertoire and function shifting the balance of cell subsets and soluble mediators toward a proinflammatory profile [ 49 , 50 , 51 ]. This results from an altered balance of key transcription factors able to promote inflammation through the induction of molecules such as TNFα , IL-6 , IL-1β , and Toll-like receptor ( TLR ) 4.…”

Section: Fatty Acids and Adipose Tissue Homeostasismentioning

confidence: 99%

Dietary Fatty Acids at the Crossroad between Obesity and Colorectal Cancer: Fine Regulators of Adipose Tissue Homeostasis and Immune Response

Cornò

Varì

Scazzocchio

et al. 2021

Cells

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Colorectal cancer (CRC) is among the major threatening diseases worldwide, being the third most common cancer, and a leading cause of death, with a global incidence expected to increase in the coming years. Enhanced adiposity, particularly visceral fat, is a major risk factor for the development of several tumours, including CRC, and represents an important indicator of incidence, survival, prognosis, recurrence rates, and response to therapy. The obesity-associated low-grade chronic inflammation is thought to be a key determinant in CRC development, with the adipocytes and the adipose tissue (AT) playing a significant role in the integration of diet-related endocrine, metabolic, and inflammatory signals. Furthermore, AT infiltrating immune cells contribute to local and systemic inflammation by affecting immune and cancer cell functions through the release of soluble mediators. Among the factors introduced with diet and enriched in AT, fatty acids (FA) represent major players in inflammation and are able to deeply regulate AT homeostasis and immune cell function through gene expression regulation and by modulating the activity of several transcription factors (TF). This review summarizes human studies on the effects of dietary FA on AT homeostasis and immune cell functions, highlighting the molecular pathways and TF involved. The relevance of FA balance in linking diet, AT inflammation, and CRC is also discussed. Original and review articles were searched in PubMed without temporal limitation up to March 2021, by using fatty acid as a keyword in combination with diet, obesity, colorectal cancer, inflammation, adipose tissue, immune cells, and transcription factors.

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Innate Lymphocytes in Adipose Tissue Homeostasis and Their Alterations in Obesity and Colorectal Cancer

Cited by 16 publications

References 59 publications

Type I Interferons as Joint Regulators of Tumor Growth and Obesity

Type I Interferons as Joint Regulators of Tumor Growth and Obesity

Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity

Dietary Fatty Acids at the Crossroad between Obesity and Colorectal Cancer: Fine Regulators of Adipose Tissue Homeostasis and Immune Response

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