scholarly journals Critical role of fatty acid metabolism in ILC2-mediated barrier protection during malnutrition and helminth infection

2016 ◽  
Vol 213 (8) ◽  
pp. 1409-1418 ◽  
Author(s):  
Christoph Wilhelm ◽  
Oliver J. Harrison ◽  
Vanessa Schmitt ◽  
Martin Pelletier ◽  
Sean P. Spencer ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Helminth Infection ◽  
Critical Role ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Environmental Signals ◽  
Essential Nutrient ◽  
Barrier Immunity

Innate lymphoid cells (ILC) play an important role in many immune processes, including control of infections, inflammation, and tissue repair. To date, little is known about the metabolism of ILC and whether these cells can metabolically adapt in response to environmental signals. Here we show that type 2 innate lymphoid cells (ILC2), important mediators of barrier immunity, predominantly depend on fatty acid (FA) metabolism during helminth infection. Further, in situations where an essential nutrient, such as vitamin A, is limited, ILC2 sustain their function and selectively maintain interleukin 13 (IL-13) production via increased acquisition and utilization of FA. Together, these results reveal that ILC2 preferentially use FAs to maintain their function in the context of helminth infection or malnutrition and propose that enhanced FA usage and FA-dependent IL-13 production by ILC2 could represent a host adaptation to maintain barrier immunity under dietary restriction.

A pro-inflammatory role of type 2 innate lymphoid cells in murine immune-mediated hepatitis

2015 ◽  
Vol 53 (12) ◽  
Author(s):  
K Karimi ◽  
K Neumann ◽  
J Meiners ◽  
R Voetlause ◽  
W Dammermann ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Immune Mediated

scholarly journals Effects of BMP7 produced by group 2 innate lymphoid cells on adipogenesis

2020 ◽  
Vol 32 (6) ◽  
pp. 407-419 ◽  
Author(s):  
Yurina Miyajima ◽  
Kafi N Ealey ◽  
Yasutaka Motomura ◽  
Miho Mochizuki ◽  
Natsuki Takeno ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Adipocyte Differentiation ◽  
Allergic Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Brown Adipocytes ◽  
Morphogenetic Protein ◽  
Group 2

Abstract Group 2 innate lymphoid cells (ILC2s) are type 2 cytokine-producing cells that have important roles in helminth infection and allergic inflammation. ILC2s are tissue-resident cells, and their phenotypes and roles are regulated by tissue-specific environmental factors. While the role of ILC2s in the lung, intestine and bone marrow has been elucidated in many studies, their role in adipose tissues is still unclear. Here, we report on the role of ILC2-derived bone morphogenetic protein 7 (BMP7) in adipocyte differentiation and lipid accumulation. Co-culture of fat-derived ILC2s with pluripotent mesenchymal C3H10T1/2 cells and committed white preadipocyte 3T3-L1 cells resulted in their differentiation to adipocytes and induced lipid accumulation. Co-culture experiments using BMP7-deficient ILC2s revealed that BMP7, produced by ILC2s, induces differentiation into brown adipocytes. Our results demonstrate that BMP7, produced by ILC2s, affects adipocyte differentiation, particularly in brown adipocytes.

The role of type 2 innate lymphoid cells in eosinophilic asthma

2019 ◽  
Vol 106 (4) ◽  
pp. 889-901 ◽  
Author(s):  
Brittany M. Salter ◽  
Michael Aw ◽  
Roma Sehmi
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Eosinophilic Asthma

scholarly journals Adaptation of Innate Lymphoid Cells to a Micronutrient Deficiency Promotes Type 2 Barrier Immunity

Science ◽  
2014 ◽  
Vol 343 (6169) ◽  
pp. 432-437 ◽  
Author(s):  
S. P. Spencer ◽  
C. Wilhelm ◽  
Q. Yang ◽  
J. A. Hall ◽  
N. Bouladoux ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Micronutrient Deficiency ◽  
Lymphoid Cells ◽  
Barrier Immunity

scholarly journals The role of type 2 innate lymphoid cells in asthma

2013 ◽  
Vol 94 (5) ◽  
pp. 933-940 ◽  
Author(s):  
Ya-Jen Chang ◽  
Rosemarie H. DeKruyff ◽  
Dale T. Umetsu
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells

scholarly journals IL-33 Drives Expansion of Type 2 Innate Lymphoid Cells and Regulatory T Cells and Protects Mice From Severe, Acute Colitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Nhi Ngo Thi Phuong ◽  
Vittoria Palmieri ◽  
Alexandra Adamczyk ◽  
Robert Klopfleisch ◽  
Jost Langhorst ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Intestinal Inflammation ◽  
Mucosal Damage ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Strong Increase ◽  
Dss Colitis

The hallmarks of inflammatory bowel disease are mucosal damage and ulceration, which are known to be high-risk conditions for the development of colorectal cancer. Recently, interleukin (IL)-33 and its receptor ST2 have emerged as critical modulators in inflammatory disorders. Even though several studies highlight the IL-33/ST2 pathway as a key factor in colitis, a detailed mode of action remains elusive. Therefore, we investigated the role of IL-33 during intestinal inflammation and its potential as a novel therapeutic target in colitis. Interestingly, the expression of IL-33, but not its receptor ST2, was significantly increased in biopsies from the inflamed colon of IBD patients compared to non-inflamed colonic tissue. Accordingly, in a mouse model of Dextran Sulfate Sodium (DSS) induced colitis, the secretion of IL-33 significantly accelerated in the colon. Induction of DSS colitis in ST2-/- mice displayed an aggravated colon pathology, which suggested a favorable role of the IL 33/ST2 pathway during colitis. Indeed, injecting rmIL-33 into mice suffering from acute DSS colitis, strongly abrogated epithelial damage, pro-inflammatory cytokine secretion, and loss of barrier integrity, while it induced a strong increase of Th2 associated cytokines (IL-13/IL-5) in the colon. This effect was accompanied by the accumulation of regulatory T cells (Tregs) and type 2 innate lymphoid cells (ILC2s) in the colon. Depletion of Foxp3+ Tregs during IL-33 treatment in DSS colitis ameliorated the positive effect on the intestinal pathology. Finally, IL-33 expanded ILC2s, which were adoptively transferred to DSS treated mice, significantly reduced colonic inflammation compared to DSS control mice. In summary, our results emphasize that the IL-33/ST2 pathway plays a crucial protective role in colitis by modulating ILC2 and Treg numbers.

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