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161 results on '"Chidgey, Ann P"'

1. The activity of early-life gene regulatory elements is hijacked in aging through pervasive AP-1-linked chromatin opening

Author

Patrick, Ralph, Naval-Sanchez, Marina, Deshpande, Nikita, Huang, Yifei, Zhang, Jingyu, Chen, Xiaoli, Yang, Ying, Tiwari, Kanupriya, Esmaeili, Mohammadhossein, Tran, Minh, Mohamed, Amin R., Wang, Binxu, Xia, Di, Ma, Jun, Bayliss, Jacqueline, Wong, Kahlia, Hun, Michael L., Sun, Xuan, Cao, Benjamin, Cottle, Denny L., Catterall, Tara, Barzilai-Tutsch, Hila, Troskie, Robin-Lee, Chen, Zhian, Wise, Andrea F., Saini, Sheetal, Soe, Ye Mon, Kumari, Snehlata, Sweet, Matthew J., Thomas, Helen E., Smyth, Ian M., Fletcher, Anne L., Knoblich, Konstantin, Watt, Matthew J., Alhomrani, Majid, Alsanie, Walaa, Quinn, Kylie M., Merson, Tobias D., Chidgey, Ann P., Ricardo, Sharon D., Yu, Di, Jardé, Thierry, Cheetham, Seth W., Marcelle, Christophe, Nilsson, Susan K., Nguyen, Quan, White, Melanie D., and Nefzger, Christian M.

Published
2024
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6. Decreased maternal serum acetate and impaired fetal thymic and regulatory T cell development in preeclampsia

Author

Hu, Mingjing, Eviston, David, Hsu, Peter, Mariño, Eliana, Chidgey, Ann, Santner-Nanan, Brigitte, Wong, Kahlia, Richards, James L., Yap, Yu Anne, Collier, Fiona, Quinton, Ann, Joung, Steven, Peek, Michael, Benzie, Ron, Macia, Laurence, Wilson, David, Ponsonby, Ann-Louise, Tang, Mimi L. K., O’Hely, Martin, Daly, Norelle L., Mackay, Charles R., Dahlstrom, Jane E., The BIS Investigator Group, Vuillermin, Peter, and Nanan, Ralph

Published
2019
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9. FOXN1GFP/w Reporter hESCs Enable Identification of Integrin-β4, HLA-DR, and EpCAM as Markers of Human PSC-Derived FOXN1+ Thymic Epithelial Progenitors

Author

Soh, Chew-Li, Giudice, Antonietta, Jenny, Robert A., Elliott, David A., Hatzistavrou, Tanya, Micallef, Suzanne J., Kianizad, Korosh, Seach, Natalie, Zúñiga-Pflücker, Juan Carlos, Chidgey, Ann P., Trounson, Alan, Nilsson, Susan K., Haylock, David N., Boyd, Richard L., Elefanty, Andrew G., and Stanley, Edouard G.

Published
2014
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22. Tolerance strategies for stem-cell-based therapies

Author

Chidgey, Ann P., Layton, Daniel, Trounson, Alan, and Boyd, Richard L.

Subjects
Evaluation, Physiological aspects, Research, Embryonic stem cells -- Physiological aspects -- Research, Biocompatibility -- Research -- Physiological aspects, Stem cell research -- Evaluation -- Physiological aspects -- Research
Abstract

There is much interest in using embryonic stem cells to regenerate tissues and organs. For this approach to succeed, these stem cells or their derivatives must engraft in patients over [...]

Published
2008

32. Autoimmune-Mediated Thymic Atrophy Is Accelerated but Reversible in RelB-Deficient Mice.

Author

O'Sullivan, Brendan J., Yekollu, Suman, Ruscher, Roland, Mehdi, Ahmed M., Maradana, Muralidhara Rao, Chidgey, Ann P., and Thomas, Ranjeny

Subjects
GENETIC polymorphisms, AUTOIMMUNE diseases, EPITHELIAL cells
Abstract

Polymorphisms impacting thymic function may decrease peripheral tolerance and hasten autoimmune disease. The NF-κB transcription factor subunit, RelB, is essential for the development and differentiation of medullary thymic epithelial cells (mTECs): RelB-deficient mice have reduced thymic cellularity and markedly fewer mTECs, lacking AIRE. The precise mechanism of this mTEC reduction in the absence of RelB is unclear. To address this, we studied mTECs and dendritic cells (DCs), which critically regulate negative selection, and thymic regulatory T-cells (tTreg) in RelB-/- mice, which have spontaneous multiorgan autoimmune disease. RelB-/- thymi were organized, with medullary structures containing AIRE-mTECs, DCs, and CD4+ thymocytes, but fewer tTreg. Granulocytes infiltrated the RelB-/- thymic cortex, capsule, and medulla, producing inflammatory thymic medullary atrophy, which could be treated by granulocyte depletion or RelB+ DC immunotherapy, with concomitant recovery of mTEC and tTreg numbers. These data indicate that central tolerance defects may be accelerated by autoimmune thymic inflammation where impaired RelB signaling impairs the medullary niche, and may be reversible by therapies enhancing peripheral Treg or suppressing inflammation. [ABSTRACT FROM AUTHOR]

Published
2018
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33. Multipotent RAG1+progenitors emerge directly from haemogenic endothelium in human pluripotent stem cell-derived haematopoietic organoids

Author

Motazedian, Ali, Bruveris, Freya F., Kumar, Santhosh V., Schiesser, Jacqueline V., Chen, Tyrone, Ng, Elizabeth S., Chidgey, Ann P., Wells, Christine A., Elefanty, Andrew G., and Stanley, Edouard G.

Abstract

Defining the ontogeny of the human adaptive immune system during embryogenesis has implications for understanding childhood diseases including leukaemias and autoimmune conditions. Using RAG1:GFP human pluripotent stem cell reporter lines, we examined human T-cell genesis from pluripotent-stem-cell-derived haematopoietic organoids. Under conditions favouring T-cell development, RAG1+ cells progressively upregulated a cohort of recognized T-cell-associated genes, arresting development at the CD4+CD8+ stage. Sort and re-culture experiments showed that early RAG1+ cells also possessed B-cell, myeloid and erythroid potential. Flow cytometry and single-cell-RNA-sequencing data showed that early RAG1+ cells co-expressed the endothelial/haematopoietic progenitor markers CD34, VECAD and CD90, whereas imaging studies identified RAG1+ cells within CD31+ endothelial structures that co-expressed SOX17+ or the endothelial marker CAV1. Collectively, these observations provide evidence for a wave of human T-cell development that originates directly from haemogenic endothelium via a RAG1+ intermediate with multilineage potential.

Published
2020
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34. Gelatin-Based 3D Microgels for In Vitro T Lineage Cell Generation

Author

Suraiya, Anisha B., Hun, Michael L., Truong, Vinh X., Forsythe, John S., and Chidgey, Ann P.

Abstract

T cells are predominantly produced by the thymus and play a significant role in maintaining our adaptive immune system. Physiological involution of the thymus occurs gradually with age, compromising naive T cell output, which can have severe clinical complications. Also, T cells are utilized as therapeutic agents in cancer immunotherapies. Therefore, there is an increasing need for strategies aimed at generating naive T cells. The majority of in vitro T cell generation studies are performed in two-dimensional (2D) cultures, which ignore the physiological thymic microenvironment and are not scalable; therefore, we applied a new three-dimensional (3D) approach. Here, we use a gelatin-based 3D microgel system for T lineage induction by co-culturing OP9-DL4 cells and mouse fetal-liver-derived hematopoietic stem cells (HSCs). Flow cytometric analysis revealed that microgel co-cultures supported T lineage induction similar to 2D cultures while providing a 3D environment. We also encapsulated mouse embryonic thymic epithelial cells (TECs) within the microgels to provide a defined 3D culture platform. The microgel system supported TEC maintenance and retained their phenotype. Together, these data show that our microgel system has the capacity for TEC maintenance and induction of in vitro T lineage differentiation with potential for scalability.

Published
2024
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36. Luteinizing Hormone-Releasing Hormone Enhances T Cell Recovery following Allogeneic Bone Marrow Transplantation1

Author

Goldberg, Gabrielle L., King, Christopher G., Nejat, Rebecca A., Suh, David Y., Smith, Odette M., Bretz, Jamison C., Samstein, Robert M., Dudakov, Jarrod A., Chidgey, Ann P., Chen-Kiang, Selina, Boyd, Richard L., and van den Brink, Marcel R. M.

Subjects
Male, Isoantigens, Mice, Inbred BALB C, T-Lymphocytes, Graft vs Tumor Effect, Graft vs Host Disease, Bone Marrow Cells, Cell Differentiation, Thymus Gland, Hematopoietic Stem Cells, Article, Gonadotropin-Releasing Hormone, Mice, Inbred C57BL, Mice, Lymphopenia, Animals, Humans, Female, Leuprolide, Spleen, Bone Marrow Transplantation
Abstract

Posttransplant immunodeficiency, specifically a lack of T cell reconstitution, is a major complication of allogeneic bone marrow transplantation. This immunosuppression results in an increase in morbidity and mortality from infections and very likely contributes to relapse. In this study, we demonstrate that sex steroid ablation using leuprolide acetate, a luteinizing hormone-releasing hormone agonist (LHRHa), increases the number of lymphoid and myeloid progenitor cells in the bone marrow and developing thymocytes in the thymus. Although few differences are observed in the peripheral myeloid compartments, the enhanced thymic reconstitution following LHRHa treatment and allogeneic bone marrow transplantation leads to enhanced peripheral T cell recovery, predominantly in the naive T cell compartment. This results in an increase in T cell function in vivo and in vitro. Graft-versus-host-disease is not exacerbated by LHRHa treatment and graft-versus-tumor activity is maintained. Because LHRHa allows for reversible (and temporary) sex steroid ablation, has a strong safety profile, and has been clinically approved for diseases such as prostate and breast cancer, this drug treatment represents a novel therapeutic approach to reversal of thymic atrophy and enhancement of immunity following immunosuppression.

Published
2009

38. Thymic Deletion and Regulatory T Cells Prevent Antimyeloperoxidase GN

Author

Tan, Diana S.Y., primary, Gan, Poh Y., additional, O’Sullivan, Kim M., additional, Hammett, Maree V., additional, Summers, Shaun A., additional, Ooi, Joshua D., additional, Lundgren, Brita A., additional, Boyd, Richard L., additional, Scott, Hamish S., additional, Kitching, A. Richard, additional, Chidgey, Ann P., additional, and Holdsworth, Stephen R., additional

Published
2013
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39. A novel Foxn1eGFP/+ mouse model identifies Bmp4-induced maintenance of Foxn1 expression and thymic epithelial progenitor populations.

Author

Barsanti, Marco, Lim, Joanna M. C., Hun, Michael L., Lister, Natalie, Wong, Kahlia, Hammett, Maree V., Lepletier, Ailin, Boyd, Richard L., Giudice, Antonietta, and Chidgey, Ann P.

Abstract

Although forkhead-box n1 (Foxn1) is a critical thymic epithelial cell regulator in thymus organogenesis, its association with epithelial differentiation and homeostasis in the postnatal and aged thymic microenvironment remains conflicting. Consequently, we have generated a Foxn1eGFP/+ knock-in mouse model that allows for refined investigation of the aging thymic epithelium. This reporter line differs from those previously published in that concomitant expression of enhanced green fluorescent protein enables live cell sorting of Foxn1+ cell populations. Our heterozygotes did not exhibit haploinsufficiency, with Foxn1 expression resembling that of wild-type mice. Comparative analysis between Foxn1 and enhanced green fluorescent protein at both the transcriptional and translational levels revealed co-localization, with progressive down-regulation observed predominantly in the aging cortical epithelium. Supplementation with bone morphogenetic protein (Bmp)-4 enhanced Foxn1 expression and colony forming efficiency in both embryonic and adult progenitor 3D cultures. Strikingly, selective maintenance of immature cortical and medullary epithelial cells was observed which is consistent with the higher Bmp receptor 2 expression levels seen in these progenitor populations. This study demonstrates the significance of our mouse model in unraveling the role of this master regulator in thymus development, homeostasis and aging, providing a faithful reporter system for phenotypic and functional investigations. [ABSTRACT FROM AUTHOR]

Published
2017
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46. Luteinizing Hormone-Releasing Hormone Enhances T Cell Recovery following Allogeneic Bone Marrow Transplantation

Author

Goldberg, Gabrielle L., primary, King, Christopher G., additional, Nejat, Rebecca A., additional, Suh, David Y., additional, Smith, Odette M., additional, Bretz, Jamison C., additional, Samstein, Robert M., additional, Dudakov, Jarrod A., additional, Chidgey, Ann P., additional, Chen-Kiang, Selina, additional, Boyd, Richard L., additional, and van den Brink, Marcel R. M., additional

Published
2009
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