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Article ; Online: Immune outposts in the adventitia: One foot in sea and one on shore.

Cautivo, Kelly M / Steer, Catherine A / Molofsky, Ari B

2020 Volume 64, Page(s) 34–41

Abstract: Advances in microscopy, genetically modified mice, and single-cell RNA sequencing have begun to deconvolute the composition and function of tissue immune niches. Here we discuss the evidence that the adventitia, the outermost layer of larger blood ... ...

Abstract	Advances in microscopy, genetically modified mice, and single-cell RNA sequencing have begun to deconvolute the composition and function of tissue immune niches. Here we discuss the evidence that the adventitia, the outermost layer of larger blood vessels, is a conserved niche and tissue immune outpost for multiple immune cells, including group 2 innate lymphoid cells (ILC2) and subsets of tissue-resident memory T cells, macrophages, and dendritic cells. We also describe the unique non-immune composition at adventitial regions, including fibroblast-like stromal cell subsets, lymphatic and blood endothelial cells, and neurons, and review how immune-stromal crosstalk impacts regional tissue immunity, organ adaptation, and disease.
MeSH term(s)	Adventitia ; Animals ; Endothelial Cells ; Humans ; Immunity, Innate ; Lymphocytes ; Mice ; Stromal Cells
Language	English
Publishing date	2020-04-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2020.03.005
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Zs.A 2773: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Circumvention of luteolysis reveals parturition pathways in mice dependent upon innate type 2 immunity.

Siewiera, Johan / McIntyre, Tara I / Cautivo, Kelly M / Mahiddine, Karim / Rideaux, Damon / Molofsky, Ari B / Erlebacher, Adrian

Immunity

2023 Volume 56, Issue 3, Page(s) 606–619.e7

Abstract: Although mice normally enter labor when their ovaries stop producing progesterone (luteolysis), parturition can also be triggered in this species through uterus-intrinsic pathways potentially analogous to the ones that trigger parturition in humans. Such ...

Abstract	Although mice normally enter labor when their ovaries stop producing progesterone (luteolysis), parturition can also be triggered in this species through uterus-intrinsic pathways potentially analogous to the ones that trigger parturition in humans. Such pathways, however, remain largely undefined in both species. Here, we report that mice deficient in innate type 2 immunity experienced profound parturition delays when manipulated endocrinologically to circumvent luteolysis, thus obliging them to enter labor through uterus-intrinsic pathways. We found that these pathways were in part driven by the alarmin IL-33 produced by uterine interstitial fibroblasts. We also implicated important roles for uterine group 2 innate lymphoid cells, which demonstrated IL-33-dependent activation prior to labor onset, and eosinophils, which displayed evidence of elevated turnover in the prepartum uterus. These findings reveal a role for innate type 2 immunity in controlling the timing of labor onset through a cascade potentially relevant to human parturition.
MeSH term(s)	Pregnancy ; Female ; Mice ; Animals ; Humans ; Interleukin-33/metabolism ; Luteolysis ; Immunity, Innate ; Myometrium/metabolism ; Lymphocytes ; Parturition/metabolism
Chemical Substances	Interleukin-33
Language	English
Publishing date	2023-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2023.01.005
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The Skinny: Pancreatic ILC2s Promote Insulin Secretion.

Cautivo, Kelly M / Molofsky, Ari B

Immunity

2017 Volume 47, Issue 5, Page(s) 812–814

Abstract: Regulation of pancreatic insulin production is pivotal in the pathophysiology and treatment of diabetes. In this issue of Immunity, Dalmas et al. (2017) describe a type 2 immune circuit where pancreatic interleukin-33 (IL-33) promotes insulin secretion ... ...

Abstract	Regulation of pancreatic insulin production is pivotal in the pathophysiology and treatment of diabetes. In this issue of Immunity, Dalmas et al. (2017) describe a type 2 immune circuit where pancreatic interleukin-33 (IL-33) promotes insulin secretion via the activity of islet-associated group 2 innate lymphoid cells (ILC2s).
MeSH term(s)	Immunity, Innate ; Insulin Secretion ; Interleukin-33 ; Lymphocytes ; Myeloid Cells ; Tretinoin
Chemical Substances	Interleukin-33 ; Tretinoin (5688UTC01R)
Language	English
Publishing date	2017-11-22
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2017.11.004
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Regulation of metabolic health and adipose tissue function by group 2 innate lymphoid cells.

Cautivo, Kelly M / Molofsky, Ari B

European journal of immunology

2016 Volume 46, Issue 6, Page(s) 1315–1325

Abstract: Adipose tissue (AT) is home to an abundance of immune cells. With chronic obesity, inflammatory immune cells accumulate and promote insulin resistance and the progression to type 2 diabetes mellitus. In contrast, recent studies have highlighted the ... ...

Abstract	Adipose tissue (AT) is home to an abundance of immune cells. With chronic obesity, inflammatory immune cells accumulate and promote insulin resistance and the progression to type 2 diabetes mellitus. In contrast, recent studies have highlighted the regulation and function of immune cells in lean, healthy AT, including those associated with type 2 or "allergic" immunity. Although traditionally activated by infection with multicellular helminthes, AT type 2 immunity is active independently of infection, and promotes tissue homeostasis, AT "browning," and systemic insulin sensitivity, protecting against obesity-induced metabolic dysfunction and type 2 diabetes mellitus. In particular, group 2 innate lymphoid cells (ILC2s) are integral regulators of AT type 2 immunity, producing the cytokines interleukin-5 and IL-13, promoting eosinophils and alternatively activated macrophages, and cooperating with and promoting AT regulatory T (Treg) cells. In this review, we focus on the recent developments in our understanding of group 2 innate lymphoid cell cells and type 2 immunity in AT metabolism and homeostasis.
MeSH term(s)	Adipose Tissue/physiology ; Adipose Tissue, Brown/physiology ; Adipose Tissue, White/physiology ; Animals ; Cell Communication ; Disease Susceptibility ; Helminthiasis/immunology ; Helminthiasis/metabolism ; Helminthiasis/parasitology ; Helminths/immunology ; Homeostasis ; Host-Parasite Interactions/immunology ; Humans ; Immunity ; Immunity, Innate ; Immunomodulation ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Signal Transduction
Language	English
Publishing date	2016-06
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201545562
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cell cycle dynamics and complement expression distinguishes mature haematopoietic subsets arising from hemogenic endothelium.

Zape, Joan P / Lizama, Carlos O / Cautivo, Kelly M / Zovein, Ann C

Cell cycle (Georgetown, Tex.)

2017 Volume 16, Issue 19, Page(s) 1835–1847

Abstract: The emergence of haematopoietic stem and progenitor cells (HSPCs) from hemogenic endothelium results in the formation of sizeable HSPC clusters attached to the vascular wall. We evaluate the cell cycle and proliferation of HSPCs involved in cluster ... ...

Abstract	The emergence of haematopoietic stem and progenitor cells (HSPCs) from hemogenic endothelium results in the formation of sizeable HSPC clusters attached to the vascular wall. We evaluate the cell cycle and proliferation of HSPCs involved in cluster formation, as well as the molecular signatures from their initial appearance to the point when cluster cells are capable of adult engraftment (definitive HSCs). We uncover a non-clonal origin of HSPC clusters with differing cell cycle, migration, and cell signaling attributes. In addition, we find that the complement cascade is highly enriched in mature HSPC clusters, possibly delineating a new role for this pathway in engraftment.
MeSH term(s)	Animals ; Cell Cycle/genetics ; Cell Differentiation ; Cell Division ; Complement System Proteins/genetics ; Complement System Proteins/metabolism ; Embryo, Mammalian ; Endothelium, Vascular/cytology ; Endothelium, Vascular/growth & development ; Endothelium, Vascular/metabolism ; Female ; Flow Cytometry ; Gene Expression Regulation ; Hemangioblasts/cytology ; Hemangioblasts/metabolism ; Hematopoiesis/genetics ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Mice ; Mice, Transgenic ; Pregnancy ; Signal Transduction ; Staining and Labeling/methods
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2017-08-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2017.1361569
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Zs.A 5881: Show issues

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Article: Group 2 innate lymphoid cells constrain type 3/17 lymphocytes in shared stromal niches to restrict liver fibrosis.

Sbierski-Kind, Julia / Cautivo, Kelly M / Wagner, Johanna C / Dahlgren, Madelene W / Nilsson, Julia / Krasilnikov, Maria / Mroz, Nicholas M / Lizama, Carlos O / Gan, Anna Lu / Matatia, Peri R / Taruselli, Marcela T / Chang, Anthony A / Caryotakis, Sofia / O'Leary, Claire E / Kotas, Maya / Mattis, Aras N / Peng, Tien / Locksley, Richard M / Molofsky, Ari B

bioRxiv : the preprint server for biology

2023

Abstract: Group 2 innate lymphoid cells (ILC2s) cooperate with adaptive Th2 cells as key organizers of tissue type 2 immune responses, while a spectrum of innate and adaptive lymphocytes coordinate early type 3/17 immunity. Both type 2 and type 3/17 lymphocyte ... ...

Abstract	Group 2 innate lymphoid cells (ILC2s) cooperate with adaptive Th2 cells as key organizers of tissue type 2 immune responses, while a spectrum of innate and adaptive lymphocytes coordinate early type 3/17 immunity. Both type 2 and type 3/17 lymphocyte associated cytokines are linked to tissue fibrosis, but how their dynamic and spatial topographies may direct beneficial or pathologic organ remodelling is unclear. Here we used volumetric imaging in models of liver fibrosis, finding accumulation of periportal and fibrotic tract IL-5
Language	English
Publishing date	2023-04-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.26.537913
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Article ; Online: Dysregulated lung stroma drives emphysema exacerbation by potentiating resident lymphocytes to suppress an epithelial stem cell reservoir.

Wang, Chaoqun / Hyams, Ben / Allen, Nancy C / Cautivo, Kelly / Monahan, Kiara / Zhou, Minqi / Dahlgren, Madelene W / Lizama, Carlos O / Matthay, Michael / Wolters, Paul / Molofsky, Ari B / Peng, Tien

Immunity

2023 Volume 56, Issue 3, Page(s) 576–591.e10

Abstract: Aberrant tissue-immune interactions are the hallmark of diverse chronic lung diseases. Here, we sought to define these interactions in emphysema, a progressive disease characterized by infectious exacerbations and loss of alveolar epithelium. Single-cell ...

Abstract	Aberrant tissue-immune interactions are the hallmark of diverse chronic lung diseases. Here, we sought to define these interactions in emphysema, a progressive disease characterized by infectious exacerbations and loss of alveolar epithelium. Single-cell analysis of human emphysema lungs revealed the expansion of tissue-resident lymphocytes (TRLs). Murine studies identified a stromal niche for TRLs that expresses Hhip, a disease-variant gene downregulated in emphysema. Stromal-specific deletion of Hhip induced the topographic expansion of TRLs in the lung that was mediated by a hyperactive hedgehog-IL-7 axis. 3D immune-stem cell organoids and animal models of viral exacerbations demonstrated that expanded TRLs suppressed alveolar stem cell growth through interferon gamma (IFNγ). Finally, we uncovered an IFNγ-sensitive subset of human alveolar stem cells that was preferentially lost in emphysema. Thus, we delineate a stromal-lymphocyte-epithelial stem cell axis in the lung that is modified by a disease-variant gene and confers host susceptibility to emphysema.
MeSH term(s)	Humans ; Mice ; Animals ; Pulmonary Emphysema/genetics ; Lung ; Emphysema ; Lymphocytes ; Stem Cells ; Pulmonary Disease, Chronic Obstructive
Language	English
Publishing date	2023-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2023.01.032
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Interferon gamma constrains type 2 lymphocyte niche boundaries during mixed inflammation.

Cautivo, Kelly M / Matatia, Peri R / Lizama, Carlos O / Mroz, Nicholas M / Dahlgren, Madelene W / Yu, Xiaofei / Sbierski-Kind, Julia / Taruselli, Marcela T / Brooks, Jeremy F / Wade-Vallance, Adam / Caryotakis, Sofia E / Chang, Anthony A / Liang, Hong-Erh / Zikherman, Julie / Locksley, Richard M / Molofsky, Ari B

Immunity

2022 Volume 55, Issue 2, Page(s) 254–271.e7

Abstract: Allergic immunity is orchestrated by group 2 innate lymphoid cells (ILC2s) and type 2 helper T (Th2) cells prominently arrayed at epithelial- and microbial-rich barriers. However, ILC2s and Th2 cells are also present in fibroblast-rich niches within the ... ...

Abstract	Allergic immunity is orchestrated by group 2 innate lymphoid cells (ILC2s) and type 2 helper T (Th2) cells prominently arrayed at epithelial- and microbial-rich barriers. However, ILC2s and Th2 cells are also present in fibroblast-rich niches within the adventitial layer of larger vessels and similar boundary structures in sterile deep tissues, and it remains unclear whether they undergo dynamic repositioning during immune perturbations. Here, we used thick-section quantitative imaging to show that allergic inflammation drives invasion of lung and liver non-adventitial parenchyma by ILC2s and Th2 cells. However, during concurrent type 1 and type 2 mixed inflammation, IFNγ from broadly distributed type 1 lymphocytes directly blocked both ILC2 parenchymal trafficking and subsequent cell survival. ILC2 and Th2 cell confinement to adventitia limited mortality by the type 1 pathogen Listeria monocytogenes. Our results suggest that the topography of tissue lymphocyte subsets is tightly regulated to promote appropriately timed and balanced immunity.
MeSH term(s)	Animals ; Cell Death/immunology ; Cell Movement/immunology ; Hypersensitivity/immunology ; Immunity, Innate ; Inflammation/immunology ; Interferon-gamma/immunology ; Interleukin-33/immunology ; Interleukin-5/metabolism ; Listeria monocytogenes ; Listeriosis/immunology ; Listeriosis/mortality ; Liver/immunology ; Lung/immunology ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Lysophospholipids/immunology ; Mice ; Parenchymal Tissue/immunology ; Sphingosine/analogs & derivatives ; Sphingosine/immunology ; Th1 Cells/immunology ; Th2 Cells/immunology ; Th2 Cells/metabolism
Chemical Substances	IFNG protein, mouse ; Interleukin-33 ; Interleukin-5 ; Lysophospholipids ; sphingosine 1-phosphate (26993-30-6) ; Interferon-gamma (82115-62-6) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2022-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2021.12.014
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Autoregulation of insulin receptor signaling through MFGE8 and the αvβ5 integrin.

Datta, Ritwik / Lizama, Carlos O / Soltani, Amin K / Mckleroy, William / Podolsky, Michael J / Yang, Christopher D / Huynh, Tony L / Cautivo, Kelly M / Wang, Biao / Koliwad, Suneil K / Abumrad, Nada A / Atabai, Kamran

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 18

Abstract: The role of integrins, in particular αv integrins, in regulating insulin resistance is incompletely understood. We have previously shown that the αvβ5 integrin ligand milk fat globule epidermal growth factor like 8 (MFGE8) regulates cellular uptake of ... ...

Abstract	The role of integrins, in particular αv integrins, in regulating insulin resistance is incompletely understood. We have previously shown that the αvβ5 integrin ligand milk fat globule epidermal growth factor like 8 (MFGE8) regulates cellular uptake of fatty acids. In this work, we evaluated the impact of MFGE8 on glucose homeostasis. We show that acute blockade of the MFGE8/β5 pathway enhances while acute augmentation dampens insulin-stimulated glucose uptake. Moreover, we find that insulin itself induces cell-surface enrichment of MFGE8 in skeletal muscle, which then promotes interaction between the αvβ5 integrin and the insulin receptor leading to dampening of skeletal-muscle insulin receptor signaling. Blockade of the MFGE8/β5 pathway also enhances hepatic insulin sensitivity. Our work identifies an autoregulatory mechanism by which insulin-stimulated signaling through its cognate receptor is terminated through up-regulation of MFGE8 and its consequent interaction with the αvβ5 integrin, thereby establishing a pathway that can potentially be targeted to improve insulin sensitivity.
MeSH term(s)	Animals ; Antigens, CD/genetics ; Antigens, Surface/genetics ; Fatty Acids/genetics ; Fatty Acids/metabolism ; Glucose/metabolism ; Glycolipids/genetics ; Glycoproteins/genetics ; Homeostasis/genetics ; Humans ; Insulin/genetics ; Insulin Resistance/genetics ; Integrin alphaVbeta3/genetics ; Lipid Droplets ; Mice ; Milk Proteins/genetics ; Muscle, Skeletal/metabolism ; Receptor, Insulin/genetics ; Receptors, Vitronectin/genetics ; Signal Transduction/genetics
Chemical Substances	Antigens, CD ; Antigens, Surface ; Fatty Acids ; Glycolipids ; Glycoproteins ; Insulin ; Integrin alphaVbeta3 ; Mfge8 protein, mouse ; Milk Proteins ; Receptors, Vitronectin ; integrin alphaVbeta5 ; milk fat globule ; INSR protein, human (EC 2.7.10.1) ; Receptor, Insulin (EC 2.7.10.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-04-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2102171118
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Zs.A 1148: Show issues

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Article ; Online: CNS fibroblasts form a fibrotic scar in response to immune cell infiltration.

Dorrier, Cayce E / Aran, Dvir / Haenelt, Ezekiel A / Sheehy, Ryan N / Hoi, Kimberly K / Pintarić, Lucija / Chen, Yanan / Lizama, Carlos O / Cautivo, Kelly M / Weiner, Geoffrey A / Popko, Brian / Fancy, Stephen P J / Arnold, Thomas D / Daneman, Richard

Nature neuroscience

2021 Volume 24, Issue 2, Page(s) 234–244

Abstract: Fibrosis is a common pathological response to inflammation in many peripheral tissues and can prevent tissue regeneration and repair. Here, we identified persistent fibrotic scarring in the CNS following immune cell infiltration in the experimental ... ...

Abstract	Fibrosis is a common pathological response to inflammation in many peripheral tissues and can prevent tissue regeneration and repair. Here, we identified persistent fibrotic scarring in the CNS following immune cell infiltration in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis. Using lineage tracing and single-cell sequencing in EAE, we determined that the majority of the fibrotic scar is derived from proliferative CNS fibroblasts, not pericytes or infiltrating bone marrow-derived cells. Ablating proliferating fibrotic cells using cell-specific expression of herpes thymidine kinase led to an increase in oligodendrocyte lineage cells within the inflammatory lesions and a reduction in motor disability. We further identified that interferon-gamma pathway genes are enriched in CNS fibrotic cells, and the fibrotic cell-specific deletion of Ifngr1 resulted in reduced fibrotic scarring in EAE. These data delineate a framework for understanding the CNS fibrotic response.
MeSH term(s)	Animals ; Blood-Brain Barrier/pathology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Fibroblasts/pathology ; Fibrosis/pathology ; Mice ; Neutrophil Infiltration ; Oligodendroglia/pathology ; Spinal Cord/pathology
Language	English
Publishing date	2021-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-020-00770-9
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