scholarly journals The essential function of IL-33 in metabolic regulation

2020 ◽  
Vol 52 (7) ◽  
pp. 768-775 ◽  
Author(s):  
Wenping Li ◽  
Yiyuan Li ◽  
Jin Jin
Keyword(s):  
Metabolic Regulation ◽  
Underlying Mechanism ◽  
Lymphoid Cells ◽  
Regulatory Function ◽  
Current Evidence ◽  
Metabolic Processes ◽  
Interleukin 33 ◽  
Health And Disease ◽  
Essential Function ◽  
Group 2

Abstract Interleukin-33 (IL-33) is produced by various types of cells under physical or pathological conditions. As a multifunctional partner in health and disease, current evidence reveals that IL-33 also participates in several metabolic processes. IL-33 has been proven to contribute to regulating the activity of ST2+ group 2 innate lymphoid cells and regulatory T cells in adipose, which leads to the shift of insulin sensitivity and glucose clearance in glucose metabolism, thermogenesis, and adipocyte beiging in adipose metabolism. In this review, we briefly summarize the biological characteristics of Il-33 and discuss its regulatory function in glucose and adipose metabolism. By clarifying the underlying mechanism of IL-33, we highlight the crosstalk between immune response and metabolic processes mediated by IL-33.

scholarly journals Mepolizumab in the management of severe eosinophilic asthma in adults: current evidence and practical experience

2016 ◽  
Vol 11 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Gilda Varricchi ◽  
Diego Bagnasco ◽  
Matteo Ferrando ◽  
Francesca Puggioni ◽  
Giovanni Passalacqua ◽  
...  
Keyword(s):  
Practical Experience ◽  
Lymphoid Cells ◽  
Th2 Cells ◽  
Current Evidence ◽  
Blood Leukocytes ◽  
Eosinophilic Asthma ◽  
Gm Csf ◽  
Severe Eosinophilic Asthma ◽  
Nk T Cells ◽  
Group 2

Eosinophils represent approximately 1% of peripheral blood leukocytes in normal donors and their maturation and differentiation in the bone marrow are mainly regulated by interleukin (IL)-5 [Broughton et al. 2015]. IL-5, a cytokine that belongs to the β common-chain family, together with IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF), stimulates also the activation and survival of eosinophils and, to some extent, of basophils. IL-5 binds to a heterodimer receptor composed of the specific subunit IL-5Rα and a common subunit βc shared with IL-3 and GM-CSF. Human eosinophils express approximately a three-fold higher level of IL-5Rα compared with basophils. Major sources of IL-5 are T-helper 2 (Th2) cells, mast cells, CD34+ progenitor cells, invariant natural killer (NK) T-cells, group 2 innate lymphoid cells (ILC2s), and eosinophils themselves. ILC2s control not only eosinophil number but also their circadian cycling through the production of IL-5.

Human innate lymphoid cells

Blood ◽  
2014 ◽  
Vol 124 (5) ◽  
pp. 700-709 ◽  
Author(s):  
Mette D. Hazenberg ◽  
Hergen Spits
Keyword(s):  
Interferon Γ ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Interleukin 5 ◽  
Type 2 Cytokines ◽  
Lymphoid Tissue Inducer Cells ◽  
Health And Disease ◽  
Group 2 ◽  
And Function ◽  
Regulatory Functions

Innate lymphoid cells (ILCs) are lymphoid cells that do not express rearranged receptors and have important effector and regulatory functions in innate immunity and tissue remodeling. ILCs are categorized into 3 groups based on their distinct patterns of cytokine production and the requirement of particular transcription factors for their development and function. Group 1 ILCs (ILC1s) produce interferon γ and depend on Tbet, group 2 ILCs (ILC2s) produce type 2 cytokines like interleukin-5 (IL-5) and IL-13 and require GATA3, and group 3 ILCs (ILC3s) include lymphoid tissue inducer cells, produce IL-17 and/or IL-22, and are dependent on RORγt. Whereas ILCs play essential roles in the innate immune system, uncontrolled activation and proliferation of ILCs can contribute to inflammatory autoimmune diseases. In this review, we provide an overview of the characteristics of ILCs in the context of health and disease. We will focus on human ILCs but refer to mouse studies if needed to clarify aspects of ILC biology.

scholarly journals Acetylcholine production by group 2 innate lymphoid cells promotes mucosal immunity to helminths

2021 ◽  
Vol 6 (57) ◽  
pp. eabd0359
Author(s):  
Luke B. Roberts ◽  
Corinna Schnoeller ◽  
Rita Berkachy ◽  
Matthew Darby ◽  
Jamie Pillaye ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Mucosal Barrier ◽  
Nippostrongylus Brasiliensis ◽  
Interleukin 33 ◽  
Group 2 ◽  
Maximal Induction

Innate lymphoid cells (ILCs) are critical mediators of immunological and physiological responses at mucosal barrier sites. Whereas neurotransmitters can stimulate ILCs, the synthesis of small-molecule neurotransmitters by these cells has only recently been appreciated. Group 2 ILCs (ILC2s) are shown here to synthesize and release acetylcholine (ACh) during parasitic nematode infection. The cholinergic phenotype of pulmonary ILC2s was associated with their activation state, could be induced by in vivo exposure to extracts of Alternaria alternata or the alarmin cytokines interleukin-33 (IL-33) and IL-25, and was augmented by IL-2 in vitro. Genetic disruption of ACh synthesis by murine ILC2s resulted in increased parasite burdens, lower numbers of ILC2s, and reduced lung and gut barrier responses to Nippostrongylus brasiliensis infection. These data demonstrate a functional role for ILC2-derived ACh in the expansion of ILC2s for maximal induction of type 2 immunity.

scholarly journals The metabolism-modulating activity of IL-17 signaling in health and disease

2021 ◽  
Vol 218 (5) ◽  
Author(s):  
Rami Bechara ◽  
Mandy J. McGeachy ◽  
Sarah L. Gaffen
Keyword(s):  
Signal Transduction ◽  
Metabolic Regulation ◽  
Metabolic Processes ◽  
Health And Disease

IL-17 was discovered nearly 30 yr ago, but it has only been recently appreciated that a key function of this cytokine is to orchestrate cellular and organismal metabolism. Indeed, metabolic regulation is integrated into both the physiological and the pathogenic aspects of IL-17 responses. Thus, understanding the interplay between IL-17 and downstream metabolic processes could ultimately inform therapeutic opportunities for diseases involving IL-17, including some not traditionally linked to this cytokine pathway. Here, we discuss the emerging pathophysiological roles of IL-17 related to cellular and organismal metabolism, including metabolic regulation of IL-17 signal transduction.

scholarly journals ILC2 Activation by Protozoan Commensal Microbes

2019 ◽  
Vol 20 (19) ◽  
pp. 4865 ◽  
Author(s):  
Kyle Burrows ◽  
Louis Ngai ◽  
Flora Wong ◽  
David Won ◽  
Arthur Mortha
Keyword(s):  
Intestinal Tract ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Immune Homeostasis ◽  
Current Field ◽  
Bacterial Microbiome ◽  
Health And Disease ◽  
Group 2

Group 2 innate lymphoid cells (ILC2s) are a member of the ILC family and are involved in protective and pathogenic type 2 responses. Recent research has highlighted their involvement in modulating tissue and immune homeostasis during health and disease and has uncovered critical signaling circuits. While interactions of ILC2s with the bacterial microbiome are rather sparse, other microbial members of our microbiome, including helminths and protozoans, reveal new and exciting mechanisms of tissue regulation by ILC2s. Here we summarize the current field on ILC2 activation by the tissue and immune environment and highlight particularly new intriguing pathways of ILC2 regulation by protozoan commensals in the intestinal tract.

scholarly journals Emerging Roles of Interleukin-33-responsive Kidney Group 2 Innate Lymphoid Cells in Acute Kidney Injury

2020 ◽  
Vol 21 (4) ◽  
pp. 1544
Author(s):  
Wei-Yu Chen ◽  
Lung-Chih Li ◽  
Yi-Hsiu Wu ◽  
Jenq-Lin Yang ◽  
Hong-Tai Tzeng
Keyword(s):  
Acute Kidney Injury ◽  
Immune Cells ◽  
Kidney Injury ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Immune Functions ◽  
Loss Of Function ◽  
Interleukin 33 ◽  
Group 2 ◽  
Preclinical Animal Models

Interleukin (IL)-33, a member of the IL-1 family of cytokines, is involved in innate and adaptive immune responses. IL-33 triggers pleiotropic immune functions in multiple types of immune cells, which express the IL-33 receptor, ST2. Recent studies have revealed the potential applications of IL-33 for treating acute kidney injury in preclinical animal models. However, IL-33 and IL-33-responding immune cells are reported to exhibit both detrimental and beneficial roles. The IL-33-mediated immunomodulatory functions have been investigated using loss-of-function approaches, such as IL33-deficient mice, IL-33 antagonists, or administration of exogenous IL-33 recombinant protein. This review will discuss the key findings on IL-33-mediated activation of kidney resident group 2 innate lymphoid cells (ILC2s) and summarize the current understanding of the differential functions of endogenous IL-33 and exogenous IL-33 and their potential implications in treating acute kidney injury.

scholarly journals IL-33 genetics and epigenetics in immune-related diseases

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Eleonora Di Salvo ◽  
Marco Casciaro ◽  
Sebastiano Gangemi
Keyword(s):  
Secretory Pathway ◽  
Interleukin 1 ◽  
Lymphoid Cells ◽  
Th2 Cells ◽  
Interleukin 33 ◽  
Immune Genes ◽  
Helminthic Infections ◽  
Type 2 Immune Response ◽  
Group 2 ◽  
Diverse Data

AbstractInterleukin-33 (IL-33) is a 30KDa protein, which belongs to the Interleukin-1 cytokine family. It is a crucial regulator of innate and adaptive immune responses. This interleukin is additionally involved in the inflammatory reaction versus helminthic infections. Interleukin 33 acts on group 2 innate lymphoid cells and mast cells macrophages, dendritic cells and CD4 + Th2 cells eliciting a type 2 immune response. Moreover, the cytokine can activate the ST2 of Tregs, demonstrating its ability to downregulate inflammation. IL-33 has also an intracellular function by regulating transcription. The active IL-33 doesn’t have a signal peptide, so it’s not released across a normal secretory pathway; the interleukin is released when the cells are damages and acts like an “alarmin”. Its influence on immune activation could be slightly adjusted via fine epigenetic interactions involving cascade pathways and immune genes. Due to the diverse data emerged from different experimental research, we decided span literature to clarify, as much as possible, how IL-33 is influenced by and influence gene expression. The authors reported how its balance is influenced, according to the tissue considered. Fundamental for immune-related diseases, IL-33 has a key role in controlling inflammation. The understanding of the cytokine switch will be fundamental in a near future in order to block or activate some immune pathways. In fact, we could control interleukins effects not only by monoclonal antibodies but also by using siRNA or miRNAs for silencing or expressing key genes.

scholarly journals c-Rel Is Required for IL-33-Dependent Activation of ILC2s

2021 ◽  
Vol 12 ◽  
Author(s):  
Aidil Zaini ◽  
Thomas S. Fulford ◽  
Raelene J. Grumont ◽  
Jessica Runting ◽  
Grace Rodrigues ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Cytokine Production ◽  
Control Point ◽  
Cell Types ◽  
Lymphoid Cells ◽  
Central Control ◽  
Critical Component ◽  
Interleukin 33 ◽  
Group 2 ◽  
And Function

Group 2 innate lymphoid cells (ILC2s) are emerging as important cellular regulators of homeostatic and disease-associated immune processes. The cytokine interleukin-33 (IL-33) promotes ILC2-dependent inflammation and immunity, with IL-33 having been shown to activate NF-κB in a wide variety of cell types. However, it is currently unclear which NF-κB members play an important role in IL-33-dependent ILC2 biology. Here, we identify the NF-κB family member c-Rel as a critical component of the IL-33-dependent activation of ILC2s. Although c-Rel is dispensable for ILC2 development, it is critical for ILC2 function in the lung, with c-Rel-deficient (c-Rel–/–) mice present a significantly reduced response to papain- and IL-33-induced lung inflammation. We also show that the absence of c-Rel reduces the IL-33-dependent expansion of ILC2 precursors and lower levels of IL-5 and IL-13 cytokine production by mature ILC2s in the lung. Together, these results identify the IL-33-c-Rel axis as a central control point of ILC2 activation and function.

scholarly journals Stromal cells maintain immune cell homeostasis in adipose tissue via production of interleukin-33

2019 ◽  
Vol 4 (35) ◽  
pp. eaax0416 ◽  
Author(s):  
T. Mahlakõiv ◽  
A.-L. Flamar ◽  
L. K. Johnston ◽  
S. Moriyama ◽  
G. G. Putzel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Progenitor Cells ◽  
Stromal Cells ◽  
Immune Cell ◽  
Cell Activity ◽  
Lymphoid Cells ◽  
Immune Homeostasis ◽  
Low Grade ◽  
Interleukin 33 ◽  
Group 2

Obesity is driven by chronic low-grade inflammation resulting from dysregulated immune cell accumulation and function in white adipose tissue (WAT). Interleukin-33 (IL-33) is a key cytokine that controls innate and adaptive immune cell activity and immune homeostasis in WAT, although the sources of IL-33 have remained controversial. Here, we show that WAT-resident mesenchyme-derived stromal cells are the dominant producers of IL-33. Adipose stem and progenitor cells (ASPCs) produced IL-33 in all WAT depots, whereas mesothelial cells served as an additional source of IL-33 in visceral WAT. ASPC-derived IL-33 promoted a regulatory circuit that maintained an immune tone in WAT via the induction of group 2 innate lymphoid cell–derived type 2 cytokines and maintenance of eosinophils, whereas mesothelial IL-33 also acted as an alarmin by inducing peritoneal immune response upon infection. Together, these data reveal a previously unrecognized regulatory network between tissue-resident progenitor cells and innate lymphoid cells that maintains immune homeostasis in adipose tissue.

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