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28 results on '"Newland, Stephen A."'

1. Early intermittent hyperlipidaemia alters tissue macrophages to fuel atherosclerosis

Author

Takaoka, Minoru, Zhao, Xiaohui, Lim, Hwee Ying, Magnussen, Costan G., Ang, Owen, Suffee, Nadine, Schrank, Patricia R., Ong, Wei Siong, Tsiantoulas, Dimitrios, Sommer, Felix, Mohanta, Sarajo K., Harrison, James, Meng, Yaxing, Laurans, Ludivine, Wu, Feitong, Lu, Yuning, Masters, Leanne, Newland, Stephen A., Denti, Laura, Hong, Mingyang, Chajadine, Mouna, Juonala, Markus, Koskinen, Juhani S., Kähönen, Mika, Pahkala, Katja, Rovio, Suvi P., Mykkänen, Juha, Thomson, Russell, Kaisho, Tsuneyasu, Habenicht, Andreas J. R., Clement, Marc, Tedgui, Alain, Ait-Oufella, Hafid, Zhao, Tian X., Nus, Meritxell, Ruhrberg, Christiana, Taleb, Soraya, Williams, Jesse W., Raitakari, Olli T., Angeli, Véronique, and Mallat, Ziad

Published
2024
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4. Marginal zone B cells produce ‘natural’ atheroprotective IgM antibodies in a T cell–dependent manner

Author

Harrison, James, primary, Newland, Stephen A, additional, Jiang, Wei, additional, Giakomidi, Despoina, additional, Zhao, Xiaohui, additional, Clement, Marc, additional, Masters, Leanne, additional, Corovic, Andrej, additional, Zhang, Xian, additional, Drago, Fabrizio, additional, Ma, Marcella, additional, Ozsvar Kozma, Maria, additional, Yasin, Froher, additional, Saady, Yuta, additional, Kothari, Hema, additional, Zhao, Tian X, additional, Shi, Guo-Ping, additional, McNamara, Coleen A, additional, Binder, Christoph J, additional, Sage, Andrew P, additional, Tarkin, Jason M, additional, Mallat, Ziad, additional, and Nus, Meritxell, additional

Published
2024
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9. Marginal Zone B cells produce 'natural' atheroprotective IgM antibodies in a T-cell-dependent manner

Author

Harrison, James, primary, Newland, Stephen, additional, Jiang, Wei, additional, Zhao, Xiaohui, additional, Clement, Marc, additional, Masters, Leanne, additional, Corovic, Andrej, additional, Zhang, Xian, additional, Drago, Fabrizio, additional, Ma, Marcella, additional, Kozma, Maria Ozsvar, additional, Yasin, Froher, additional, Saady, Yuta, additional, Kothari, Hema, additional, Zhao, Tian, additional, Shi, Guo-Ping, additional, McNamara, Coleen, additional, Binder, Christoph, additional, Sage, Andrew, additional, Tarkin, Jason, additional, Mallat, Ziad, additional, and Nus, Meritxell, additional

Published
2022
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10. Validated germline-competent embryonic stem cell lines from nonobese diabetic mice

Author

Nichols, Jennifer, Jones, Kenneth, Phillips, Jenny M., Newland, Stephen A., Roode, Mila, Mansfield, William, Smith, Austin, and Cooke, Anne

Subjects
Animal models in research -- Usage, Genetically modified mice -- Models, Embryonic stem cells -- Health aspects, Embryonic stem cells -- Research, Type 1 diabetes -- Genetic aspects, Type 1 diabetes -- Research
Abstract

Nonobese diabetic (NOD) mice provide an excellent model of type 1 diabetes. The genetic contribution to this disease is complex, with more than 20 loci implicated in diabetes onset. One of the challenges for researchers using the NOD mouse model (and, indeed, other models of spontaneous autoimmune disease) has been the high density of sequence variation within candidate chromosomal segments. Furthermore, the scope for analyzing many putative disease loci via gene targeting has been hampered by the lack of NOD embryonic stem (ES) cells. We describe here the derivation of NOD ES cell lines capable of generating chimeric mice after stable genetic modification. These NOD ES cell lines also show efficient germline transmission, with offspring developing diabetes. The availability of these cells will not only enable the dissection of closely linked loci and the role they have in the onset of type 1 diabetes but also facilitate the generation of new transgenics., Type 1 diabetes is an autoimmune disease in which pancreatic beta cells are selectively destroyed. The development of this disease is known to be governed by both genetic and environmental [...]

Published
2009

11. 2019 ATVB Plenary Lecture: Interleukin-2 Therapy in Cardiovascular Disease: The Potential to Regulate Innate and Adaptive Immunity

Author

Zhao, Tian X, Newland, Stephen A, Mallat, Ziad, Mallat, Ziad [0000-0003-0443-7878], and Apollo - University of Cambridge Repository

Subjects
Interleukin-13, interleukin, Adaptive Immunity, T-Lymphocytes, Regulatory, cytokines, Immunity, Innate, myocardial infarction, cardiovascular disease, Cardiovascular Diseases, Animals, Humans, Interleukin-2, atherosclerosis, Interleukin-5
Abstract

Regulatory T cells and type-2 innate lymphoid cells represent 2 subsets of immune cells, which have been shown in preclinical models to be important in atherosclerosis and myocardial repair. Regulatory T cells play a crucial role in immune homeostasis and tolerance via their interactions with effector T cells, dendritic cells, and monocytes/macrophages. They also utilize and secrete inhibitory cytokines, including interleukin 10 and transforming growth factor β, to regulate or suppress pathogenic immune responses. Type-2 innate lymphoid cells have an important role in type-2 immune responses and tissue repair through secreting interleukins 5 and 13, as well as a variety of biological mediators and growth factors. Intriguingly, interleukin-2 has emerged as a common cytokine, which can be harnessed to upregulate both cell types, and also has important translational consequences as clinical trials are ongoing for its use in cardiovascular disease. Here, we briefly review the biology of these regulatory immune cell types, discuss the preclinical and clinical evidence for their functions in cardiovascular disease, examine the prospects for clinical translation and current ongoing trials, and finally, postulate how overlap in the mechanisms of upregulation may be leveraged in future treatments for patients.

Published
2020
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12. Interleukin-33 Signaling Controls the Development of Iron-Recycling Macrophages

Author

Lu, Yuning, primary, Basatemur, Gemma, additional, Scott, Ian C., additional, Chiarugi, Davide, additional, Clement, Marc, additional, Harrison, James, additional, Jugdaohsingh, Ravin, additional, Yu, Xian, additional, Newland, Stephen A., additional, Jolin, Helen E., additional, Li, Xuan, additional, Chen, Xiao, additional, Szymanska, Monika, additional, Haraldsen, Guttorm, additional, Palmer, Gaby, additional, Fallon, Padraic G., additional, Cohen, E. Suzanne, additional, McKenzie, Andrew N.J., additional, and Mallat, Ziad, additional

Published
2020
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14. MARK4 (Microtubule Affinity-Regulating Kinase 4)-Dependent Inflammasome Activation Promotes Atherosclerosis-Brief Report

Author

Clement, Marc, Chen, Xiao, Chenoweth, Hannah L, Teng, Zhongzhao, Thome, Sarah, Newland, Stephen A, Harrison, James, Yu, Xian, Finigan, Alison J, Mallat, Ziad, Li, Xuan, Teng, Zhongzhao [0000-0003-3973-6157], Harrison, James [0000-0003-4960-5062], Mallat, Ziad [0000-0003-0443-7878], Li, Xuan [0000-0002-0754-3011], and Apollo - University of Cambridge Repository

Subjects
Aged, 80 and over, Male, Inflammasomes, Interleukin-18, Middle Aged, Protein Serine-Threonine Kinases, Atherosclerosis, microtubules, Mice, Inbred C57BL, Mice, NLRP3, Receptors, LDL, MARK4, inflammasome, inflammation, NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Humans, bone marrow cells, Cells, Cultured, Aged
Abstract

OBJECTIVE: MARK4 (microtubule affinity-regulating kinase 4) regulates NLRP3 (nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain containing 3) inflammasome activation. The aim of the study is to examine the role of MARK4 in hematopoietic cells during atherosclerosis. METHODS AND RESULTS: We show increased MARK4 expression in human atherosclerotic lesions compared with adjacent areas. MARK4 is coexpressed with NLRP3, and they colocalize in areas enriched in CD68-positive but α-SMA (α-smooth muscle actin)-negative cells. Expression of MARK4 and NLRP3 in the atherosclerotic lesions is associated with the production of active IL (interleukin)-1β and IL-18. To directly assess the role of hematopoietic MARK4 in NLRP3 inflammasome activation and atherosclerotic plaque formation, Ldlr (low-density lipoprotein receptor)-deficient mice were lethally irradiated and reconstituted with either wild-type or Mark4-deficient bone marrow cells, and were subsequently fed a high-fat diet and cholesterol diet for 9 weeks. Mark4 deficiency in bone marrow cells led to a significant reduction of lesion size, together with decreased circulating levels of IL-18 and IFN-γ (interferon-γ). Furthermore, Mark4 deficiency in primary murine bone marrow-derived macrophages prevented cholesterol crystal-induced NLRP3 inflammasome activation, as revealed by reduced caspase-1 activity together with reduced production of IL-1β and IL-18. CONCLUSIONS: MARK4-dependent NLRP3 inflammasome activation in the hematopoietic cells regulates the development of atherosclerosis.

Published
2019

15. Impaired Autophagy in CD11b + Dendritic Cells Expands CD4 + Regulatory T Cells and Limits Atherosclerosis in Mice

Author

Clement, Marc, primary, Raffort, Juliette, additional, Lareyre, Fabien, additional, Tsiantoulas, Dimitrios, additional, Newland, Stephen, additional, Lu, Yuning, additional, Masters, Leanne, additional, Harrison, James, additional, Saveljeva, Svetlana, additional, Ma, Marcella K.L., additional, Ozsvar-Kozma, Maria, additional, Lam, Brian Y.H., additional, Yeo, Giles S.H., additional, Binder, Christoph J., additional, Kaser, Arthur, additional, and Mallat, Ziad, additional

Published
2019
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17. Marginal Zone B cells control follicular helper T cell response to high cholesterol diet

Author

Nus, Meritxell, primary, Sage, Andy P., additional, Lu, Yuning, additional, Masters, Leanne, additional, Lam, Brian Yh, additional, Newland, Stephen, additional, Weller, Sandra, additional, Tsiantoulas, Dimitrios, additional, Raffort, Juliette, additional, Marcus, Damienne, additional, Finigan, Alison, additional, Kitt, Lauren, additional, Figg, Nichola, additional, Schirmbeck, Reinhold, additional, Kneilling, Manfred, additional, Yeo, Giles Sh, additional, Binder, Christoph J., additional, De La Pompa, Jose L., additional, and Mallat, Ziad, additional

Published
2017
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19. Type-2 innate lymphoid cells control the development of atherosclerosis in mice

Author

Newland, Stephen A., primary, Mohanta, Sarajo, additional, Clément, Marc, additional, Taleb, Soraya, additional, Walker, Jennifer A., additional, Nus, Meritxell, additional, Sage, Andrew P., additional, Yin, Changjun, additional, Hu, Desheng, additional, Kitt, Lauren L., additional, Finigan, Alison J., additional, Rodewald, Hans-Reimer, additional, Binder, Christoph J., additional, McKenzie, Andrew N. J., additional, Habenicht, Andreas J., additional, and Mallat, Ziad, additional

Published
2017
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20. Marginal zone B cells control the response of follicular helper T cells to a high-cholesterol diet

Author

Nus, Meritxell, primary, Sage, Andrew P, additional, Lu, Yuning, additional, Masters, Leanne, additional, Lam, Brian Y H, additional, Newland, Stephen, additional, Weller, Sandra, additional, Tsiantoulas, Dimitrios, additional, Raffort, Juliette, additional, Marcus, Damiënne, additional, Finigan, Alison, additional, Kitt, Lauren, additional, Figg, Nichola, additional, Schirmbeck, Reinhold, additional, Kneilling, Manfred, additional, Yeo, Giles S H, additional, Binder, Christoph J, additional, de la Pompa, José Luis, additional, and Mallat, Ziad, additional

Published
2017
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21. 2019 ATVBPlenary Lecture

Author

Zhao, Tian X., Newland, Stephen A., and Mallat, Ziad

Abstract

Regulatory T cells and type-2 innate lymphoid cells represent 2 subsets of immune cells, which have been shown in preclinical models to be important in atherosclerosis and myocardial repair. Regulatory T cells play a crucial role in immune homeostasis and tolerance via their interactions with effector T cells, dendritic cells, and monocytes/macrophages. They also utilize and secrete inhibitory cytokines, including interleukin 10 and transforming growth factor β, to regulate or suppress pathogenic immune responses. Type-2 innate lymphoid cells have an important role in type-2 immune responses and tissue repair through secreting interleukins 5 and 13, as well as a variety of biological mediators and growth factors. Intriguingly, interleukin-2 has emerged as a common cytokine, which can be harnessed to upregulate both cell types, and also has important translational consequences as clinical trials are ongoing for its use in cardiovascular disease. Here, we briefly review the biology of these regulatory immune cell types, discuss the preclinical and clinical evidence for their functions in cardiovascular disease, examine the prospects for clinical translation and current ongoing trials, and finally, postulate how overlap in the mechanisms of upregulation may be leveraged in future treatments for patients.

Published
2020
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25. Copy number of FCGR3B, which is associated with systemic lupus erythematosus, correlates with protein expression and immune complex uptake

Author

Willcocks, Lisa C., primary, Lyons, Paul A., additional, Clatworthy, Menna R., additional, Robinson, James I., additional, Yang, Wanling, additional, Newland, Stephen A., additional, Plagnol, Vincent, additional, McGovern, Naomi N., additional, Condliffe, Alison M., additional, Chilvers, Edwin R., additional, Adu, Dwomoa, additional, Jolly, Elaine C., additional, Watts, Richard, additional, Lau, Yu Lung, additional, Morgan, Ann W., additional, Nash, Gerard, additional, and Smith, Kenneth G.C., additional

Published
2008
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28. Copy number of FCGR3B, which is associated with systemic lupus erythematosus, correlates with protein expression and immune complex uptake

Author

Willcocks, Lisa C, Lyons, Paul A, Clatworthy, Menna R, Robinson, James I, Yang, Wanling, Newland, Stephen A, Plagnol, Vincent, McGovern, Naomi N, Condliffe, Alison M, Chilvers, Edwin R, Adu, Dwomoa, Jolly, Elaine C, Watts, Richard, Lau, Yu Lung, Morgan, Ann W, Nash, Gerard, and Smith, Kenneth GC

Subjects
Male, Vasculitis, Neutrophils, Receptors, IgG, Gene Dosage, Genetic Variation, Autoimmunity, Antigen-Antibody Complex, GPI-Linked Proteins, White People, 3. Good health, Antibodies, Antineutrophil Cytoplasmic, Gene Expression Regulation, Humans, Lupus Erythematosus, Systemic, Female, Genetic Predisposition to Disease
Abstract

Copy number (CN) variation (CNV) has been shown to be common in regions of the genome coding for immune-related genes, and thus impacts upon polygenic autoimmunity. Low CN of FCGR3B has recently been associated with systemic lupus erythematosus (SLE). FcgammaRIIIb is a glycosylphosphatidylinositol-linked, low affinity receptor for IgG found predominantly on human neutrophils. We present novel data demonstrating that both in a family with FcgammaRIIIb-deficiency and in the normal population, FCGR3B CNV correlates with protein expression, with neutrophil uptake of and adherence to immune complexes, and with soluble serum FcgammaRIIIb. Reduced FcgammaRIIIb expression is thus likely to contribute to the impaired clearance of immune complexes, which is a feature of SLE, explaining the association between low FCGR3B CNV and SLE that we have confirmed in a Caucasian population. In contrast, antineutrophil cytoplasmic antibody-associated systemic vasculitis (AASV), a disease not associated with immune complex deposition, is associated with high FCGR3B CN. Thus, we define a role for FCGR3B CNV in immune complex clearance, a function that may explain why low FCGR3B CNV is associated with SLE, but not AASV. This is the first report of an association between disease-related gene CNV and variation in protein expression and function that may contribute to autoimmune disease susceptibility.

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