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Article ; Online: Regulation of pulmonary plasma cell responses during secondary infection with influenza virus.

MacLean, Andrew J / Bonifacio, Joao P P L / Oram, Sophia L / Mohsen, Mona O / Bachmann, Martin F / Arnon, Tal I

2024 Volume 221, Issue 7

Abstract: During secondary infection with influenza virus, plasma cells (PCs) develop within the lung, providing a local source of antibodies. However, the site and mechanisms that regulate this process are poorly defined. Here, we show that while circulating ... ...

Abstract	During secondary infection with influenza virus, plasma cells (PCs) develop within the lung, providing a local source of antibodies. However, the site and mechanisms that regulate this process are poorly defined. Here, we show that while circulating memory B cells entered the lung during rechallenge and were activated within inducible bronchus-associated lymphoid tissues (iBALTs), resident memory B (BRM) cells responded earlier, and their activation occurred in a different niche: directly near infected alveoli. This process required NK cells but was largely independent of CD4 and CD8 T cells. Innate stimuli induced by virus-like particles containing ssRNA triggered BRM cell differentiation in the absence of cognate antigen, suggesting a low threshold of activation. In contrast, expansion of PCs in iBALTs took longer to develop and was critically dependent on CD4 T cells. Our work demonstrates that spatially distinct mechanisms evolved to support pulmonary secondary PC responses, and it reveals a specialized function for BRM cells as guardians of the alveoli.
MeSH term(s)	Animals ; Plasma Cells/immunology ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/virology ; Lung/immunology ; Lung/virology ; Lung/pathology ; Mice ; CD4-Positive T-Lymphocytes/immunology ; Mice, Inbred C57BL ; Killer Cells, Natural/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation/immunology ; Memory B Cells/immunology ; Lymphocyte Activation/immunology ; Orthomyxoviridae/immunology ; Orthomyxoviridae/physiology
Language	English
Publishing date	2024-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20232014
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Article ; Online: Small habitat matrix: How does it work?

Ng, Casey Keat-Chuan / Payne, John / Oram, Felicity

Ambio

2020 Volume 50, Issue 3, Page(s) 601–614

Abstract: We present herein our perspective of a novel Small Habitats Matrix (SHM) concept showing how small habitats on private lands are untapped but can be valuable for mitigating ecological degradation. Grounded by the realities in Sabah, Malaysian Borneo, we ... ...

Abstract	We present herein our perspective of a novel Small Habitats Matrix (SHM) concept showing how small habitats on private lands are untapped but can be valuable for mitigating ecological degradation. Grounded by the realities in Sabah, Malaysian Borneo, we model a discontinuous "stepping stones" linkage that includes both terrestrial and aquatic habitats to illustrate exactly how the SHM can be deployed. Taken together, the SHM is expected to optimize the meta-population vitality in monoculture landscapes for aerial, arboreal, terrestrial and aquatic wildlife communities. We also provide the tangible cost estimates and discuss how such a concept is both economically affordable and plausible to complement global conservation initiatives. By proposing a practical approach to conservation in the rapidly developing tropics, we present a perspective from "ground zero" that reaches out to fellow scientists, funders, activists and pro-environmental land owners who often ask, "What more can we do?"
MeSH term(s)	Animals ; Animals, Wild ; Biodiversity ; Borneo ; Conservation of Natural Resources ; Ecosystem
Language	English
Publishing date	2020-09-11
Publishing country	Sweden
Document type	Journal Article
ZDB-ID	120759-3
ISSN	1654-7209 ; 0044-7447
ISSN (online)	1654-7209
ISSN	0044-7447
DOI	10.1007/s13280-020-01384-y
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Article ; Online: Interferon-γ couples CD8

Uhl, Lion F K / Cai, Han / Oram, Sophia L / Mahale, Jagdish N / MacLean, Andrew J / Mazet, Julie M / Piccirilli, Theo / He, Alexander J / Lau, Doreen / Elliott, Tim / Gerard, Audrey

Nature communications

2023 Volume 14, Issue 1, Page(s) 6727

Abstract: Effective responses to intracellular pathogens are characterized by T cell clones with a broad affinity range for their cognate peptide and diverse functional phenotypes. How T cell clones are selected throughout the response to retain a breadth of ... ...

Abstract	Effective responses to intracellular pathogens are characterized by T cell clones with a broad affinity range for their cognate peptide and diverse functional phenotypes. How T cell clones are selected throughout the response to retain a breadth of avidities remains unclear. Here, we demonstrate that direct sensing of the cytokine IFN-γ by CD8
MeSH term(s)	Interferon-gamma/genetics ; CD8-Positive T-Lymphocytes ; Cytokines ; Cell Differentiation/genetics ; Peptides
Chemical Substances	Interferon-gamma (82115-62-6) ; Cytokines ; Peptides
Language	English
Publishing date	2023-10-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-42455-4
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Article ; Online: Islet autoantibodies as precision diagnostic tools to characterize heterogeneity in type 1 diabetes: a systematic review.

Communications medicine

2024 Volume 4, Issue 1, Page(s) 66

Abstract: Background: Islet autoantibodies form the foundation for type 1 diabetes (T1D) diagnosis and staging, but heterogeneity exists in T1D development and presentation. We hypothesized that autoantibodies can identify heterogeneity before, at, and after T1D ... ...

Abstract	Background: Islet autoantibodies form the foundation for type 1 diabetes (T1D) diagnosis and staging, but heterogeneity exists in T1D development and presentation. We hypothesized that autoantibodies can identify heterogeneity before, at, and after T1D diagnosis, and in response to disease-modifying therapies. Methods: We systematically reviewed PubMed and EMBASE databases (6/14/2022) assessing 10 years of original research examining relationships between autoantibodies and heterogeneity before, at, after diagnosis, and in response to disease-modifying therapies in individuals at-risk or within 1 year of T1D diagnosis. A critical appraisal checklist tool for cohort studies was modified and used for risk of bias assessment. Results: Here we show that 152 studies that met extraction criteria most commonly characterized heterogeneity before diagnosis (91/152). Autoantibody type/target was most frequently examined, followed by autoantibody number. Recurring themes included correlations of autoantibody number, type, and titers with progression, differing phenotypes based on order of autoantibody seroconversion, and interactions with age and genetics. Only 44% specifically described autoantibody assay standardization program participation. Conclusions: Current evidence most strongly supports the application of autoantibody features to more precisely define T1D before diagnosis. Our findings support continued use of pre-clinical staging paradigms based on autoantibody number and suggest that additional autoantibody features, particularly in relation to age and genetic risk, could offer more precise stratification. To improve reproducibility and applicability of autoantibody-based precision medicine in T1D, we propose a methods checklist for islet autoantibody-based manuscripts which includes use of precision medicine MeSH terms and participation in autoantibody standardization workshops.
Language	English
Publishing date	2024-04-06
Publishing country	England
Document type	Journal Article
ISSN	2730-664X
ISSN (online)	2730-664X
DOI	10.1038/s43856-024-00478-y
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Article ; Online: Applying a genetic risk score model to enhance prediction of future multiple sclerosis diagnosis at first presentation with optic neuritis.

Loginovic, Pavel / Wang, Feiyi / Li, Jiang / Ferrat, Lauric / Mirshahi, Uyenlinh L / Rao, H Shanker / Petzold, Axel / Tyrrell, Jessica / Green, Harry D / Weedon, Michael N / Ganna, Andrea / Tuomi, Tiinamaija / Carey, David J / Oram, Richard A / Braithwaite, Tasanee

Nature communications

2024 Volume 15, Issue 1, Page(s) 1415

Abstract: Optic neuritis (ON) is associated with numerous immune-mediated inflammatory diseases, but 50% patients are ultimately diagnosed with multiple sclerosis (MS). Differentiating MS-ON from non-MS-ON acutely is challenging but important; non-MS ON often ... ...

Abstract	Optic neuritis (ON) is associated with numerous immune-mediated inflammatory diseases, but 50% patients are ultimately diagnosed with multiple sclerosis (MS). Differentiating MS-ON from non-MS-ON acutely is challenging but important; non-MS ON often requires urgent immunosuppression to preserve vision. Using data from the United Kingdom Biobank we showed that combining an MS-genetic risk score (GRS) with demographic risk factors (age, sex) significantly improved MS prediction in undifferentiated ON; one standard deviation of MS-GRS increased the Hazard of MS 1.3-fold (95% confidence interval 1.07-1.55, P < 0.01). Participants stratified into quartiles of predicted risk developed incident MS at rates varying from 4% (95%CI 0.5-7%, lowest risk quartile) to 41% (95%CI 33-49%, highest risk quartile). The model replicated across two cohorts (Geisinger, USA, and FinnGen, Finland). This study indicates that a combined model might enhance individual MS risk stratification, paving the way for precision-based ON treatment and earlier MS disease-modifying therapy.
MeSH term(s)	Humans ; Genetic Risk Score ; Multiple Sclerosis/diagnosis ; Multiple Sclerosis/genetics ; Multiple Sclerosis/complications ; Optic Neuritis/diagnosis ; Optic Neuritis/genetics ; Optic Neuritis/complications ; Risk Factors ; Finland
Language	English
Publishing date	2024-02-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-44917-9
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Article ; Online: Type 1 Diabetes Genetic Risk in 109,954 Veterans With Adult-Onset Diabetes: The Million Veteran Program (MVP).

Diabetes care

2024

Abstract: Objective: To characterize high type 1 diabetes (T1D) genetic risk in a population where type 2 diabetes (T2D) predominates.: Research design and methods: Characteristics typically associated with T1D were assessed in 109,594 Million Veteran Program ... ...

Abstract	Objective: To characterize high type 1 diabetes (T1D) genetic risk in a population where type 2 diabetes (T2D) predominates. Research design and methods: Characteristics typically associated with T1D were assessed in 109,594 Million Veteran Program participants with adult-onset diabetes, 2011-2021, who had T1D genetic risk scores (GRS) defined as low (0 to <45%), medium (45 to <90%), high (90 to <95%), or highest (≥95%). Results: T1D characteristics increased progressively with higher genetic risk (P < 0.001 for trend). A GRS ≥ 90% was more common with diabetes diagnoses before age 40 years, but 95% of those participants were diagnosed at age ≥40 years, and they resembled T2D in mean age (64.3 years) and BMI (32.3 kg/m2). Compared with the low risk group, the highest-risk group was more likely to have diabetic ketoacidosis (low 0.9% vs. highest GRS 3.7%), hypoglycemia prompting emergency visits (3.7% vs. 5.8%), outpatient plasma glucose <50 mg/dL (7.5% vs. 13.4%), a shorter median time to start insulin (3.5 vs. 1.4 years), use of a T1D diagnostic code (16.3% vs. 28.1%), low C-peptide levels if tested (1.8% vs. 32.4%), and glutamic acid decarboxylase antibodies (6.9% vs. 45.2%), all P < 0.001. Conclusions: Characteristics associated with T1D were increased with higher genetic risk, and especially with the top 10% of risk. However, the age and BMI of those participants resemble people with T2D, and a substantial proportion did not have diagnostic testing or use of T1D diagnostic codes. T1D genetic screening could be used to aid identification of adult-onset T1D in settings in which T2D predominates.
Language	English
Publishing date	2024-04-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	441231-x
ISSN	1935-5548 ; 0149-5992
ISSN (online)	1935-5548
ISSN	0149-5992
DOI	10.2337/dc23-1927
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Zs.A 1434: 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: Interferon-γ couples CD8+ T cell avidity and differentiation during infection

Lion F. K. Uhl / Han Cai / Sophia L. Oram / Jagdish N. Mahale / Andrew J. MacLean / Julie M. Mazet / Theo Piccirilli / Alexander J. He / Doreen Lau / Tim Elliott / Audrey Gerard

Nature Communications, Vol 14, Iss 1, Pp 1-

2023 Volume 17

Abstract: Abstract Effective responses to intracellular pathogens are characterized by T cell clones with a broad affinity range for their cognate peptide and diverse functional phenotypes. How T cell clones are selected throughout the response to retain a breadth ...

Abstract	Abstract Effective responses to intracellular pathogens are characterized by T cell clones with a broad affinity range for their cognate peptide and diverse functional phenotypes. How T cell clones are selected throughout the response to retain a breadth of avidities remains unclear. Here, we demonstrate that direct sensing of the cytokine IFN-γ by CD8+ T cells coordinates avidity and differentiation during infection. IFN-γ promotes the expansion of low-avidity T cells, allowing them to overcome the selective advantage of high-avidity T cells, whilst reinforcing high-avidity T cell entry into the memory pool, thus reducing the average avidity of the primary response and increasing that of the memory response. IFN-γ in this context is mainly provided by virtual memory T cells, an antigen-inexperienced subset with memory features. Overall, we propose that IFN-γ and virtual memory T cells fulfil a critical immunoregulatory role by enabling the coordination of T cell avidity and fate.
Keywords	Science ; Q
Subject code	612
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Disease-modifying therapies and features linked to treatment response in type 1 diabetes prevention: a systematic review.

Felton, Jamie L / Griffin, Kurt J / Oram, Richard A / Speake, Cate / Long, S Alice / Onengut-Gumuscu, Suna / Rich, Stephen S / Monaco, Gabriela S F / Evans-Molina, Carmella / DiMeglio, Linda A / Ismail, Heba M / Steck, Andrea K / Dabelea, Dana / Johnson, Randi K / Urazbayeva, Marzhan / Gitelman, Stephen / Wentworth, John M / Redondo, Maria J / Sims, Emily K

Communications medicine

2023 Volume 3, Issue 1, Page(s) 130

Abstract: Background: Type 1 diabetes (T1D) results from immune-mediated destruction of insulin-producing beta cells. Prevention efforts have focused on immune modulation and supporting beta cell health before or around diagnosis; however, heterogeneity in ... ...

Abstract	Background: Type 1 diabetes (T1D) results from immune-mediated destruction of insulin-producing beta cells. Prevention efforts have focused on immune modulation and supporting beta cell health before or around diagnosis; however, heterogeneity in disease progression and therapy response has limited translation to clinical practice, highlighting the need for precision medicine approaches to T1D disease modification. Methods: To understand the state of knowledge in this area, we performed a systematic review of randomized-controlled trials with ≥50 participants cataloged in PubMed or Embase from the past 25 years testing T1D disease-modifying therapies and/or identifying features linked to treatment response, analyzing bias using a Cochrane-risk-of-bias instrument. Results: We identify and summarize 75 manuscripts, 15 describing 11 prevention trials for individuals with increased risk for T1D, and 60 describing treatments aimed at preventing beta cell loss at disease onset. Seventeen interventions, mostly immunotherapies, show benefit compared to placebo (only two prior to T1D onset). Fifty-seven studies employ precision analyses to assess features linked to treatment response. Age, beta cell function measures, and immune phenotypes are most frequently tested. However, analyses are typically not prespecified, with inconsistent methods of reporting, and tend to report positive findings. Conclusions: While the quality of prevention and intervention trials is overall high, the low quality of precision analyses makes it difficult to draw meaningful conclusions that inform clinical practice. To facilitate precision medicine approaches to T1D prevention, considerations for future precision studies include the incorporation of uniform outcome measures, reproducible biomarkers, and prespecified, fully powered precision analyses into future trial design.
Language	English
Publishing date	2023-10-05
Publishing country	England
Document type	Journal Article
ISSN	2730-664X
ISSN (online)	2730-664X
DOI	10.1038/s43856-023-00357-y
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Article: Tangier disease and ABCA1.

Oram, J F

Biochimica et biophysica acta

2000 Volume 1529, Issue 1-3, Page(s) 321–330

Abstract: Tangier disease is an autosomal recessive genetic disorder characterized by a severe high-density lipoprotein (HDL) deficiency, sterol deposition in tissue macrophages, and prevalent atherosclerosis. Mutations in the ATP binding cassette transporter ... ...

Abstract	Tangier disease is an autosomal recessive genetic disorder characterized by a severe high-density lipoprotein (HDL) deficiency, sterol deposition in tissue macrophages, and prevalent atherosclerosis. Mutations in the ATP binding cassette transporter ABCA1 cause Tangier disease and other familial HDL deficiencies. ABCA1 controls a cellular pathway that secretes cholesterol and phospholipids to lipid-poor apolipoproteins. This implies that an inability of newly synthesized apolipoproteins to acquire cellular lipids by the ABCA1 pathway leads to their rapid degradation and an over-accumulation of cholesterol in macrophages. Thus, ABCA1 plays a critical role in modulating flux of tissue cholesterol and phospholipids into the reverse cholesterol transport pathway, making it an important therapeutic target for clearing excess cholesterol from macrophages and preventing atherosclerosis.
MeSH term(s)	ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/chemistry ; ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Apolipoproteins/metabolism ; Biological Transport ; Gene Expression Regulation ; Homozygote ; Humans ; Lipoproteins, HDL/metabolism ; Liver/metabolism ; Macrophages/metabolism ; Models, Chemical ; Models, Molecular ; Mutation ; Tangier Disease/genetics ; Tangier Disease/metabolism
Chemical Substances	ABCA1 protein, human ; ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters ; Apolipoproteins ; Lipoproteins, HDL
Language	English
Publishing date	2000-10-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/s1388-1981(00)00157-8
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Article: Novel approaches to treating cardiovascular disease: lessons from Tangier disease.

Oram, J F

Expert opinion on investigational drugs

2000 Volume 10, Issue 3, Page(s) 427–438

Abstract: Atherosclerotic cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in Western societies. Although cholesterol is a major CVD risk factor, therapeutic interventions to lower plasma cholesterol levels have had limited success ...

Abstract	Atherosclerotic cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in Western societies. Although cholesterol is a major CVD risk factor, therapeutic interventions to lower plasma cholesterol levels have had limited success in reducing coronary events. Thus, novel approaches are needed to reduce or eliminate CVD. A potential therapeutic target is a newly discovered ATP binding cassette transporter called ABCA1, a cell membrane protein that is the gateway for secretion of excess cholesterol from macrophages into the high density lipoprotein (HDL) metabolic pathway. Mutations in ABCA1 cause Tangier disease, a severe HDL deficiency syndrome characterised by accumulation of cholesterol in tissue macrophages and prevalent atherosclerosis. Studies of Tangier disease heterozygotes revealed that the relative activity of ABCA1 determines plasma HDL levels and susceptibility to CVD. Drugs that induce ABCA1 in mice increase clearance of cholesterol from tissues and inhibit intestinal absorption of dietary cholesterol. Thus, ABCA1-stimulating drugs have the potential to both mobilise cholesterol from atherosclerotic lesions and eliminate cholesterol from the body. By reducing plaque formation and rupture independently of the atherogenic factors involved, these drugs would be powerful agents for treating CVD.
MeSH term(s)	Animals ; Cardiovascular Diseases/blood ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/genetics ; Humans ; Lipoproteins, LDL/genetics ; Lipoproteins, LDL/physiology ; Tangier Disease/blood ; Tangier Disease/drug therapy ; Tangier Disease/genetics
Chemical Substances	Lipoproteins, LDL
Language	English
Publishing date	2000-11-16
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1182884-5
ISSN	1744-7658 ; 1354-3784 ; 0967-8298
ISSN (online)	1744-7658
ISSN	1354-3784 ; 0967-8298
DOI	10.1517/13543784.10.3.427
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