Elia D. Tait Wojno

University of Washington

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Christopher A. Hunter

University of Pennsylvania

David Artis

Cornell University

Oyebola O. Oyesola

National Institute of Allergy and Infectious Diseases

Lauren M. Webb

University of Manchester

Tajie H. Harris

University of Virginia

Mark C. Siracusa

Rutgers New Jersey Medical School

Simon P. Früh

Cornell University

David S. Roos

University of Pennsylvania

Lisa C. Osborne

University of British Columbia

Kathryn Ruymann

Thomas Jefferson University

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University of Pennsylvania

102

Cornell University

New York State College of Veterinary Medicine

California University of Pennsylvania

University of Washington

National Institutes of Health

Children's Hospital of Philadelphia

Institute of Immunology

Harvard University

Philadelphia University

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TSLP-mediated extramedullary hematopoiesis promotes allergic inflammation (P4473)

The Journal of Immunology (2013)

Mark C. Siracusa Elia D. Tait Wojno Lisa C. Osborne Steven A. Saenz Brian Kim

Abstract Extramedullary hematopoiesis (EMH) refers to the differentiation of hematopoietic stem cells (HSCs) into effector cells that occurs in compartments outside of the bone marrow. Previous studies established a link between pattern recognition receptor-expressing HSCs, EMH and innate immune responses to bacterial or viral pathogens. However, the factors that regulate EMH and whether EMH is a conserved mechanism of innate immunity to diverse stimuli remain poorly defined. Here, we demonstrate a previously unrecognized role for thymic stromal lymphopoietin (TSLP) in promoting the population expansion of Lineage-, CD34+, c-Kit+ granulocyte-monocyte progenitor (GMP)-like cells in the periphery. TSLP-elicited progenitors possess the capacity to differentiate into macrophages, mast cells and basophils. Critically, adoptive transfer of TSLP-elicited GMP-like cells was sufficient to promote Th2 cytokine-dependent immunity to an intestinal helminth parasite, demonstrating a role for TSLP-elicited GMP-like cells in promoting inflammation. Further, circulating progenitor cells were also increased in allergic patients with a gain-of-function polymorphism in TSLP, suggesting that the TSLP-EMH pathway may be operational in human disease. These data demonstrate a previously unrecognized role for TSLP in promoting EMH that contributes to the development of Th2-cytokine-mediated inflammation and identify the TSLP-EMH pathway as a possible therapeutic target to treat allergic inflammation.

Thymic stromal lymphopoietin

Allergic Inflammation

Innate lymphoid cell

Adoptive Cell Transfer

10.4049/jimmunol.190.supp.52.4

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Citations (0)

Thymic stromal lymphopoietin–elicited basophil responses promote eosinophilic esophagitis

Nature Medicine (2013)

Mario Noti Elia D. Tait Wojno Brian Kim Mark C. Siracusa Paul Giacomin

Thymic stromal lymphopoietin

Eosinophilic Esophagitis

Pathogenesis

10.1038/nm.3281

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Citations (377)

T Cells in Early Osteoarthritis

Springer eBooks (2021)

Laura E. Keller Lisa A. Fortier Elia D. Tait Wojno

Transdifferentiation

Synovial joint

10.1007/978-3-030-79485-9_11

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Citations (1)

Label-Free Imaging of Eosinophilic Esophagitis Mouse Models Using Optical Coherence Tomography

Methods in molecular biology (2016)

Aneesh Alex Elia D. Tait Wojno David Artis Chao Zhou

Eosinophilic Esophagitis

Pathophysiology

Ex vivo

10.1007/978-1-4939-3603-8_12

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Citations (2)

Single Cell Analysis Reveals Multi-faceted miR-375 Regulation of the Intestinal Crypt

bioRxiv (Cold Spring Harbor Laboratory) (2020)

Michael T. Shanahan Matt Kanke Ajeet P. Singh Jonathan Villanueva Adrian J. McNairn

Summary The role of individual miRNAs in small intestinal (SI) epithelial homeostasis is under-explored. In this study, we discovered that miR-375 is among the most enriched miRNAs in intestinal crypts and stem cells (ISCs), especially facultative ISCs. We then showed by multiple manipulations, including CRISPR/Cas9 editing, that miR-375 is strongly suppressed by Wnt-signaling. Single-cell RNA-seq analysis of SI crypt-enriched cells from miR-375 knockout (375-KO) mice revealed elevated numbers of tuft cells and increased expression of pro-proliferative genes in ISCs. Accordingly, the genetic loss of miR-375 promoted resistance to helminth infection and enhanced the regenerative response to irradiation. The conserved effects of miR-375 were confirmed by gain-of-function studies in Drosophila midgut stem cells in vivo. Moreover, functional experiments in enteroids uncovered a regulatory relationship between miR-375 and Yap1 that controls cell survival. Finally, analysis of mouse model and clinical data revealed an inverse association between miR-375 levels and intestinal tumor development. Highlights miR-375 is one of the most enriched miRNAs in ISCs, especially facultative ISCs. miR-375 modifies tuft cell abundance and pro-proliferative gene expression in ISCs. Loss of miR-375 in mice enhances the host response to helminth infection and crypt regeneration. Mouse and human intestinal cancer are associated with reduced miR-375 expression. eTOC Blurb Sethupathy and colleagues show that miR-375 is a Wnt-responsive, ISC-enriched miRNA that serves as a break on intestinal crypt proliferation. They also show that miR-375 modulates tuft cell abundance and pro-proliferative gene expression in ISCs, that miR-375 loss enhances the host response to helminth infection as well as crypt regeneration post-irradiation, and its reduced expression is associated with intestinal cancer.

LGR5

YAP1

Planarian

Intestinal epithelium

10.1101/2020.10.01.321612

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Citations (4)

Dynamic evolution of regulatory element ensembles in primate CD4+ T cells

Nature Ecology & Evolution (2018)

Charles G. Danko Lauren A. Choate Brooke A. Marks Edward J. Rice Zhong Wang

Transcription

Conserved sequence

10.1038/s41559-017-0447-5

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Citations (69)

The Cytokines Interleukin 27 and Interferon-γ Promote Distinct Treg Cell Populations Required to Limit Infection-Induced Pathology

Immunity (2012)

Aisling O’Hara Hall Daniel P. Beiting Cristina M. Tato Beena John Guillaume Oldenhove

CXCR3

Adoptive Cell Transfer

10.1016/j.immuni.2012.06.014

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Citations (325)

Arginase 1 is an innate lymphoid-cell-intrinsic metabolic checkpoint controlling type 2 inflammation

Nature Immunology (2016)

Laurel A. Monticelli Michael D. Buck Anne-Laure Flamar Steven A. Saenz Elia D. Tait Wojno

Innate lymphoid cell

Proinflammatory cytokine

10.1038/ni.3421

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Citations (254)

Basophils Promote Innate Lymphoid Cell Responses in Inflamed Skin

The Journal of Immunology (2014)

Brian Kim Kelvin Wang Mark C. Siracusa Steven A. Saenz Jonathan R. Brestoff

Type 2 inflammation underlies allergic diseases such as atopic dermatitis, which is characterized by the accumulation of basophils and group 2 innate lymphoid cells (ILC2s) in inflamed skin lesions. Although murine studies have demonstrated that cutaneous basophil and ILC2 responses are dependent on thymic stromal lymphopoietin, whether these cell populations interact to regulate the development of cutaneous type 2 inflammation is poorly defined. In this study, we identify that basophils and ILC2s significantly accumulate in inflamed human and murine skin and form clusters not observed in control skin. We demonstrate that murine basophil responses precede ILC2 responses and that basophils are the dominant IL-4-enhanced GFP-expressing cell type in inflamed skin. Furthermore, basophils and IL-4 were necessary for the optimal accumulation of ILC2s and induction of atopic dermatitis-like disease. We show that ILC2s express IL-4Rα and proliferate in an IL-4-dependent manner. Additionally, basophil-derived IL-4 was required for cutaneous ILC2 responses in vivo and directly regulated ILC2 proliferation ex vivo. Collectively, these data reveal a previously unrecognized role for basophil-derived IL-4 in promoting ILC2 responses during cutaneous inflammation.

Thymic stromal lymphopoietin

Innate lymphoid cell

Allergic Inflammation

Interleukin 33

10.4049/jimmunol.1401307

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Citations (253)

Exercising Immunity: Interleukin-13 Flexes Muscle

Immunity (2020)

Lauren M. Webb Elia D. Tait Wojno

Reprogramming

Interleukin 15

10.1016/j.immuni.2020.05.012

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Citations (2)