scholarly journals Group 2 innate lymphoid cells support hematopoietic recovery under stress conditions

2021 ◽  
Vol 218 (5) ◽  
Author(s):  
Takao Sudo ◽  
Yasutaka Motomura ◽  
Daisuke Okuzaki ◽  
Tetsuo Hasegawa ◽  
Takafumi Yokota ◽  
...  
Keyword(s):  
B Cell ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Stress Conditions ◽  
Hematopoietic Stem ◽  
Gm Csf ◽  
Induced Stress ◽  
Hematopoietic Recovery ◽  
Group 2 ◽  
Resident Group

The cell-cycle status of hematopoietic stem and progenitor cells (HSPCs) becomes activated following chemotherapy-induced stress, promoting bone marrow (BM) regeneration; however, the underlying molecular mechanism remains elusive. Here we show that BM-resident group 2 innate lymphoid cells (ILC2s) support the recovery of HSPCs from 5-fluorouracil (5-FU)–induced stress by secreting granulocyte-macrophage colony-stimulating factor (GM-CSF). Mechanistically, IL-33 released from chemo-sensitive B cell progenitors activates MyD88-mediated secretion of GM-CSF in ILC2, suggesting the existence of a B cell–ILC2 axis for maintaining hematopoietic homeostasis. GM-CSF knockout mice treated with 5-FU showed severe loss of myeloid lineage cells, causing lethality, which was rescued by transferring BM ILC2s from wild-type mice. Further, the adoptive transfer of ILC2s to 5-FU–treated mice accelerates hematopoietic recovery, while the reduction of ILC2s results in the opposite effect. Thus, ILC2s may function by “sensing” the damaged BM spaces and subsequently support hematopoietic recovery under stress conditions.

scholarly journals Activation of group 2 innate lymphoid cells alleviates aging-associated cognitive decline

2020 ◽  
Vol 217 (4) ◽  
Author(s):  
Ivan Ting Hin Fung ◽  
Poornima Sankar ◽  
Yuanyue Zhang ◽  
Lisa S. Robison ◽  
Xiuli Zhao ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Brain Physiology ◽  
Aged Brain ◽  
Group 2 ◽  
Resident Group ◽  
And Function

Increasing evidence has challenged the traditional view about the immune privilege of the brain, but the precise roles of immune cells in regulating brain physiology and function remain poorly understood. Here, we report that tissue-resident group 2 innate lymphoid cells (ILC2) accumulate in the choroid plexus of aged brains. ILC2 in the aged brain are long-lived, are relatively resistant to cellular senescence and exhaustion, and are capable of switching between cell cycle dormancy and proliferation. They are functionally quiescent at homeostasis but can be activated by IL-33 to produce large amounts of type 2 cytokines and other effector molecules in vitro and in vivo. Intracerebroventricular transfer of activated ILC2 revitalized the aged brain and enhanced the cognitive function of aged mice. Administration of IL-5, a major ILC2 product, was sufficient to repress aging-associated neuroinflammation and alleviate aging-associated cognitive decline. Targeting ILC2 in the aged brain may provide new avenues to combat aging-associated neurodegenerative disorders.

scholarly journals Interleukin-5–producing group 2 innate lymphoid cells control eosinophilia induced by interleukin-2 therapy

Blood ◽  
2014 ◽  
Vol 124 (24) ◽  
pp. 3572-3576 ◽  
Author(s):  
Frédéric Van Gool ◽  
Ari B. Molofsky ◽  
Malika M. Morar ◽  
Michelle Rosenzwajg ◽  
Hong-Erh Liang ◽  
...  
Keyword(s):  
Cellular Network ◽  
Low Dose ◽  
Interleukin 2 ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Interleukin 5 ◽  
Key Points ◽  
Group 2 ◽  
Resident Group

Key Points Tissue resident group 2 innate lymphoid cells are the main cells producing IL-5 and driving eosinophilia in response to low-dose IL-2 therapy. We described a novel cellular network activated during IL-2 treatment that may lead to a more efficient use of IL-2 in immunotherapy.

Influx, Persistence, and Recall of Eosinophils and GATA-3+ Innate Lymphoid Cells in the Nasal Mucosa of Mice Exposed and Reexposed to the Gaseous Air Pollutant Ozone

2019 ◽  
Vol 48 (2) ◽  
pp. 323-337
Author(s):  
Jack R. Harkema ◽  
Elyse A. Eldridge ◽  
Ryan P. Lewandowski ◽  
James G. Wagner
Keyword(s):  
B Cell ◽  
Messenger Rna ◽  
Innate Lymphoid Cells ◽  
Air Pollutant ◽  
Lymphoid Cells ◽  
Ozone Exposure ◽  
Nasal Tissue ◽  
New Findings ◽  
Group 2 ◽  
Deficient Mice

Mice exposed to the air pollutant ozone develop eosinophilic rhinitis that is mediated by group 2, GATA-3+, innate lymphoid cells (ILC2s). In the present study, we determined the influx, persistence, and recall of nasal ILC2s and eosinophils in ozone-exposed mice. C57BL/6 (T/B cell sufficient, ILC sufficient), Rag2−/− (T/B cell deficient, ILC sufficient), and Rag2−/−Il2rg−/− (T/B cell deficient, ILC deficient) mice were exposed to 0 or 0.8 ppm ozone for 1 or 9 weekdays and killed 1 or 17 days postexposure. GATA-3+ lymphocytes were sparse in nasal tissue of air-exposed ILC-sufficient mice and absent in ILC-deficient mice. Nine-day, but not 1-day, ozone exposures induced nasal influxes of eosinophils and GATA-3+ lymphocytes in C57BL/6 and Rag2−/− mice but not in Rag2−/−Il2rg−/− mice. Eosinophils waned 17 days postexposure in ILC-sufficient strains of mice. GATA-3+ lymphocytes in C57BL/6 mice also attenuated after exposure but not in ILC-sufficient Rag2−/− mice. Eosinophils, but not GATA-3+ cells, increased rapidly with reexposure in ILC-sufficient mice. Type 2 immune-related messenger RNA expression correlated with cellular responses to ozone. These new findings in mice further elucidate the role of ILC2s in ozone-induced eosinophilic rhinitis and support epidemiologic associations between ozone exposure and eosinophilic inflammation in children.

scholarly journals Tissue-Resident Group 2 Innate Lymphoid Cells Differentiate by Layered Ontogeny and In Situ Perinatal Priming

Immunity ◽  
2019 ◽  
Vol 50 (6) ◽  
pp. 1425-1438.e5 ◽  
Author(s):  
Christoph Schneider ◽  
Jinwoo Lee ◽  
Satoshi Koga ◽  
Roberto R. Ricardo-Gonzalez ◽  
Jesse C. Nussbaum ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Group 2 ◽  
Resident Group

scholarly journals Migration of Lung Resident Group 2 Innate Lymphoid Cells Link Allergic Lung Inflammation and Liver Immunity

2021 ◽  
Vol 12 ◽  
Author(s):  
Laura Mathä ◽  
Mónica Romera-Hernández ◽  
Catherine A. Steer ◽  
Yi Han Yin ◽  
Mona Orangi ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Eosinophilic Inflammation ◽  
Allergic Lung Inflammation ◽  
Pre Treatment ◽  
Group 2 ◽  
Resident Group ◽  
Type 2 Inflammation

Group 2 innate lymphoid cells (ILC2s) are tissue resident in the lung and activated by inhaled allergens via epithelial-derived alarmins including IL-33. Activated ILC2s proliferate, produce IL-5 and IL-13, and induce eosinophilic inflammation. Here, we report that intranasal IL-33 or the protease allergen papain administration resulted in increased numbers of ILC2s not only in the lung but also in peripheral blood and liver. Analyses of IL-33 treated parabiosis mice showed that the increase in lung ILC2s was due to proliferation of lung resident ILC2s, whereas the increase in liver ILC2s was due to the migration of activated lung ILC2s. Lung-derived ILC2s induced eosinophilic hepatitis and expression of fibrosis-related genes. Intranasal IL-33 pre-treatment also attenuated concanavalin A-induced acute hepatitis and cirrhosis. These results suggest that activated lung resident ILC2s emigrate from the lung, circulate, settle in the liver and promote type 2 inflammation and attenuate type 1 inflammation.

scholarly journals Group 2 Innate Lymphoid Cells Directly Induce B Cell Activation in Humans

2016 ◽  
Vol 137 (2) ◽  
pp. AB1 ◽  
Author(s):  
Richard Kasjanski ◽  
Atsushi Kato ◽  
Julie A. Poposki ◽  
Bruce S. Bochner ◽  
Yun Cao ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
B Cell Activation ◽  
Group 2

scholarly journals Group 2 innate lymphoid cells in bone marrow regulate osteoclastogenesis in a reciprocal manner via RANKL, GM-CSF and IL-13

2021 ◽  
Author(s):  
Yoshiki Momiuchi ◽  
Yasutaka Motomura ◽  
Emiko Suga ◽  
Hiroki Mizuno ◽  
Junichi Kikuta ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
M2 Macrophage ◽  
Dependent Manner ◽  
Bone Homeostasis ◽  
Rankl Expression ◽  
Peripheral Tissues ◽  
Gm Csf ◽  
Group 2

Abstract Group 2 innate lymphoid cells (ILC2s) are tissue-resident cells that play different roles in different organs by sensing surrounding environmental factors. Initially, it was thought that ILC2s in bone marrow (BM) are progenitors for systemic ILC2s, which migrate to other organs and acquire effector functions. However, accumulating evidence that ILC2s differentiate in peripheral tissues suggests that BM ILC2s may play a specific role in the BM as a unique effector per se. Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor κB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is up-regulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). BM ILC2s co-cultured with BM-derived monocyte/macrophage lineage cells (BMMs) in the presence of IL-7 induce the differentiation of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts in a RANKL-dependent manner. In contrast, BM ILC2s stimulated with IL-33 down-regulate RANKL expression and convert BMMs differentiation into M2 macrophage-like cells rather than osteoclasts by granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-13 production. Intravital imaging using two-photon microscopy revealed that a depletion of ILC2s prominently impaired in vivo osteoclast activity in an IL-7 plus ATRA-induced bone loss mouse model. These results suggest that ILC2s regulate osteoclast activation and contribute to bone homeostasis in both steady state and IL-33-induced inflammation.

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