scholarly journals A stromal cell niche sustains ILC2-mediated type-2 conditioning in adipose tissue

2019 ◽  
Vol 216 (9) ◽  
pp. 1999-2009 ◽  
Author(s):  
Batika M.J. Rana ◽  
Eric Jou ◽  
Jillian L. Barlow ◽  
Noe Rodriguez-Rodriguez ◽  
Jennifer A. Walker ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Immune Cells ◽  
Stromal Cells ◽  
Stromal Cell ◽  
Cell Stress ◽  
Lymphoid Cells ◽  
Type 2 Cytokines ◽  
Group 2 ◽  
Cell Niche

Group-2 innate lymphoid cells (ILC2), type-2 cytokines, and eosinophils have all been implicated in sustaining adipose tissue homeostasis. However, the interplay between the stroma and adipose-resident immune cells is less well understood. We identify that white adipose tissue–resident multipotent stromal cells (WAT-MSCs) can act as a reservoir for IL-33, especially after cell stress, but also provide additional signals for sustaining ILC2. Indeed, we demonstrate that WAT-MSCs also support ICAM-1–mediated proliferation and activation of LFA-1–expressing ILC2s. Consequently, ILC2-derived IL-4 and IL-13 feed back to induce eotaxin secretion from WAT-MSCs, supporting eosinophil recruitment. Thus, MSCs provide a niche for multifaceted dialogue with ILC2 to sustain a type-2 immune environment in WAT.

scholarly journals Adipocytes, Innate Immunity and Obesity: A Mini-Review

2021 ◽  
Vol 12 ◽  
Author(s):  
Alecia M. Blaszczak ◽  
Anahita Jalilvand ◽  
Willa A. Hsueh
Keyword(s):  
Adipose Tissue ◽  
Immune System ◽  
Immune Cells ◽  
Adaptive Immune System ◽  
Innate Immune ◽  
Lymphoid Cells ◽  
Innate Immune Cells ◽  
Adaptive Immune

The role of adipose tissue (AT) inflammation in obesity and its multiple related-complications is a rapidly expanding area of scientific interest. Within the last 30 years, the role of the adipocyte as an endocrine and immunologic cell has been progressively established. Like the macrophage, the adipocyte is capable of linking the innate and adaptive immune system through the secretion of adipokines and cytokines; exosome release of lipids, hormones, and microRNAs; and contact interaction with other immune cells. Key innate immune cells in AT include adipocytes, macrophages, neutrophils, and innate lymphoid cells type 2 (ILC2s). The role of the innate immune system in promoting adipose tissue inflammation in obesity will be highlighted in this review. T cells and B cells also play important roles in contributing to AT inflammation and are discussed in this series in the chapter on adaptive immunity.

scholarly journals TNF Induces the Production of Type 2 Cytokines in Human Group 2 Innate Lymphoid Cells

2019 ◽  
Vol 143 (2) ◽  
pp. AB1
Author(s):  
Atsushi Kato ◽  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Kathryn E. Hulse ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Human Group ◽  
Type 2 Cytokines ◽  
Group 2

scholarly journals IL-10 Prevents the Production of Type 2 Cytokines in Human Group 2 Innate Lymphoid Cells

2017 ◽  
Vol 139 (2) ◽  
pp. AB14
Author(s):  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Bruce K. Tan ◽  
Kathryn E. Hulse ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Human Group ◽  
Type 2 Cytokines ◽  
Group 2

scholarly journals IL-10, TGF-β, and glucocorticoid prevent the production of type 2 cytokines in human group 2 innate lymphoid cells

2018 ◽  
Vol 141 (3) ◽  
pp. 1147-1151.e8 ◽  
Author(s):  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Bruce K. Tan ◽  
Ava R. Weibman ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Human Group ◽  
Type 2 Cytokines ◽  
Group 2

scholarly journals The role of rare innate immune cells in Type 2 immune activation against parasitic helminths

Parasitology ◽  
2017 ◽  
Vol 144 (10) ◽  
pp. 1288-1301 ◽  
Author(s):  
LAUREN M. WEBB ◽  
ELIA D. TAIT WOJNO
Keyword(s):  
Immune Cells ◽  
Low Frequency ◽  
Cell Types ◽  
Innate Immune ◽  
Lymphoid Cells ◽  
Innate Immune Cells ◽  
Helminth Parasites ◽  
Parasitic Helminths ◽  
Group 2

SUMMARYThe complexity of helminth macroparasites is reflected in the intricate network of host cell types that participate in the Type 2 immune response needed to battle these organisms. In this context, adaptive T helper 2 cells and the Type 2 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13 have been the focus of research for years, but recent work has demonstrated that the innate immune system plays an essential role. Some innate immune cells that promote Type 2 immunity are relatively abundant, such as macrophages and eosinophils. However, we now appreciate that more rare cell types including group 2 innate lymphoid cells, basophils, mast cells and dendritic cells make significant contributions to these responses. These cells are found at low frequency but they are specialized to their roles – located at sites such as the skin, lung and gut, where the host combats helminth parasites. These cells respond rapidly and robustly to worm antigens and worm-induced damage to produce essential cytokines, chemokines, eicosanoids and histamine to activate damaged epithelium and to recruit other effectors. Thus, a greater understanding of how these cells operate is essential to understand how the host protects itself during helminth infection.

scholarly journals Tissue-specific pathways extrude activated ILC2s to disseminate type 2 immunity

2020 ◽  
Vol 217 (4) ◽  
Author(s):  
Roberto R. Ricardo-Gonzalez ◽  
Christoph Schneider ◽  
Chang Liao ◽  
Jinwoo Lee ◽  
Hong-Erh Liang ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymphoid Cells ◽  
Nippostrongylus Brasiliensis ◽  
Tissue Specific ◽  
Type 2 Cytokines ◽  
Receptor Profile ◽  
Small Intestinal ◽  
Group 2 ◽  
Specific Tissue

Group 2 innate lymphoid cells (ILC2s) are tissue-resident cells prominent at barrier sites. Although precursors are found in blood, mature ILC2s can enter the circulation after small intestinal perturbation by migratory helminths and move to distant tissues to influence the local reparative response. Using fate-mapping and methods to bypass the lung or intestinal phases of Nippostrongylus brasiliensis infection, we show that blood ILC2s comprise heterogeneous populations derived from distinct tissues that are dependent on alarmins matched to the receptor profile of the specific tissue ILC2s. Activation of local ILC2s by tissue-specific alarmins induced their proliferation, lymph node migration, and blood dissemination, thus systemically distributing type 2 cytokines. These studies uncover a possible mechanism by which local innate responses transition to systemic type 2 responses by extrusion of activated sentinel ILC2s from tissue into the circulation.

scholarly journals The Role of Innate Lymphoid Cells in the Regulation of Immune Homeostasis in Sepsis-Mediated Lung Inflammation

Diagnostics ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 808
Author(s):  
Yuichi Akama ◽  
Naoko Satoh-Takayama ◽  
Eiji Kawamoto ◽  
Atsushi Ito ◽  
Arong Gaowa ◽  
...  
Keyword(s):  
Septic Shock ◽  
Lung Injury ◽  
Immune Cells ◽  
Lung Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
System Response ◽  
Immune Homeostasis ◽  
Type 2 Cytokines

Septic shock/severe sepsis is a deregulated host immune system response to infection that leads to life-threatening organ dysfunction. Lung inflammation as a form of acute lung injury (ALI) is often induced in septic shock. Whereas macrophages and neutrophils have been implicated as the principal immune cells regulating lung inflammation, group two innate lymphoid cells (ILC2s) have recently been identified as a new player regulating immune homeostasis. ILC2 is one of the three major ILC subsets (ILC1s, ILC2s, and ILC3s) comprised of newly identified innate immune cells. These cells are characterized by their ability to rapidly produce type 2 cytokines. ILC2s are predominant resident ILCs and, thereby, have the ability to respond to signals from damaged tissues. ILC2s regulate the immune response, and ILC2-derived type 2 cytokines may exert protective roles against sepsis-induced lung injury. This focused review not only provides readers with new insights into the signaling mechanisms by which ILC2s modulate sepsis-induced lung inflammation, but also proposes ILC2 as a novel therapeutic target for sepsis-induced ALI.

scholarly journals TNF induces production of type 2 cytokines in human group 2 innate lymphoid cells

2020 ◽  
Vol 145 (1) ◽  
pp. 437-440.e8 ◽  
Author(s):  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Bruce K. Tan ◽  
Kathryn E. Hulse ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Human Group ◽  
Type 2 Cytokines ◽  
Group 2

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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