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Article ; Online: Epstein Barr Virus and Autoimmune Responses in Systemic Lupus Erythematosus.

Jog, Neelakshi R / James, Judith A

2021 Volume 11, Page(s) 623944

Abstract: Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease. Infections or infectious reactivation are potential triggers for initiation of autoimmunity and for SLE flares. Epstein-Barr virus (EBV) is gamma herpes virus that has been ... ...

Abstract	Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease. Infections or infectious reactivation are potential triggers for initiation of autoimmunity and for SLE flares. Epstein-Barr virus (EBV) is gamma herpes virus that has been associated with several autoimmune diseases such as SLE, multiple sclerosis, Sjogren's syndrome, and systemic sclerosis. In this review, we will discuss the recent advances regarding how EBV may contribute to immune dysregulation, and how these mechanisms may relate to SLE disease progression.
MeSH term(s)	Epstein-Barr Virus Infections/immunology ; Epstein-Barr Virus Infections/pathology ; Herpesvirus 4, Human/immunology ; Humans ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/pathology ; Sjogren's Syndrome/immunology ; Sjogren's Syndrome/pathology
Language	English
Publishing date	2021-02-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.623944
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Article ; Online: The promise of precision medicine in rheumatology.

Guthridge, Joel M / Wagner, Catriona A / James, Judith A

Nature medicine

2022 Volume 28, Issue 7, Page(s) 1363–1371

Abstract: Systemic autoimmune rheumatic diseases (SARDs) exhibit extensive heterogeneity in clinical presentation, disease course, and treatment response. Therefore, precision medicine - whereby treatment is tailored according to the underlying pathogenic ... ...

Abstract	Systemic autoimmune rheumatic diseases (SARDs) exhibit extensive heterogeneity in clinical presentation, disease course, and treatment response. Therefore, precision medicine - whereby treatment is tailored according to the underlying pathogenic mechanisms of an individual patient at a specific time - represents the 'holy grail' in SARD clinical care. Current strategies include treat-to-target therapies and autoantibody testing for patient stratification; however, these are far from optimal. Recent innovations in high-throughput 'omic' technologies are now enabling comprehensive profiling at multiple levels, helping to identify subgroups of patients who may taper off potentially toxic medications or better respond to current molecular targeted therapies. Such advances may help to optimize outcomes and identify new pathways for treatment, but there are many challenges along the path towards clinical translation. In this Review, we discuss recent efforts to dissect cellular and molecular heterogeneity across multiple SARDs and future directions for implementing stratification approaches for SARD treatment in the clinic.
MeSH term(s)	Autoantibodies ; Autoimmune Diseases ; Humans ; Precision Medicine ; Rheumatic Diseases/drug therapy ; Rheumatic Diseases/genetics ; Rheumatology
Chemical Substances	Autoantibodies
Language	English
Publishing date	2022-07-04
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-022-01880-6
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Article ; Online: Editorial: Pathogens, Pathobionts, and Autoimmunity.

Spatz, Linda A / Silverman, Gregg J / James, Judith A

Frontiers in immunology

2021 Volume 12, Page(s) 752980

MeSH term(s)	Animals ; Autoimmunity/immunology ; Bacteria/immunology ; Humans ; Viruses/immunology
Language	English
Publishing date	2021-09-08
Publishing country	Switzerland
Document type	Editorial ; Introductory Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.752980
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Article ; Online: Neutrophils isolated from systemic lupus erythematosus patients exhibit a distinct functional phenotype.

Jog, Neelakshi R / Wagner, Catriona A / Aberle, Teresa / Chakravarty, Eliza F / Arriens, Cristina / Guthridge, Joel M / James, Judith A

Frontiers in immunology

2024 Volume 15, Page(s) 1339250

Abstract: Neutrophil dysregulation, particularly of a low-density subset, is associated with systemic lupus erythematosus (SLE); however, the exact role of normal-density neutrophils in SLE remains unknown. This study compares activation and functional phenotypes ... ...

Abstract	Neutrophil dysregulation, particularly of a low-density subset, is associated with systemic lupus erythematosus (SLE); however, the exact role of normal-density neutrophils in SLE remains unknown. This study compares activation and functional phenotypes of neutrophils from SLE patients and healthy controls to determine potential contributions to SLE pathogenesis. Surface activation markers and release of neutrophil extracellular traps (NETs), granule proteins, and cytokines/chemokines were measured in resting and stimulated neutrophils from SLE patients (n=19) and healthy controls (n=10). Select miRNA and mRNA involved in neutrophil development and function were also measured. Resting SLE neutrophils exhibited fewer activation markers compared to control neutrophils, and activation markers were associated with different plasma cytokines/chemokines in SLE patients compared to healthy controls. However, activation markers increased similarly in SLE and control neutrophils following stimulation with a TLR7/8 agonist, neutrophil growth factors, and bacterial mimic. At the resting state, SLE neutrophils produced significantly more CXCL10 (IP-10), with trends toward other increased cytokines/chemokines. Following stimulation, SLE neutrophils produced fewer NETs and proinflammatory cytokines compared to control neutrophils but more MMP-8. In addition, SLE neutrophils expressed less miR130a, miR132, miR27a, and miR223. In conclusion, SLE neutrophils exhibit distinct functional responses compared to control neutrophils. These functional differences may result from differential gene expression via miRNAs. Furthermore, the differences in functional phenotype of SLE neutrophils suggest that they may contribute to SLE differently dependent on the inflammatory milieu.
MeSH term(s)	Humans ; Neutrophils/metabolism ; Lupus Erythematosus, Systemic/metabolism ; Extracellular Traps/metabolism ; Cytokines/metabolism ; Chemokines/metabolism
Chemical Substances	Cytokines ; Chemokines
Language	English
Publishing date	2024-03-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1339250
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Article ; Online: Clinical perspectives on lupus genetics: advances and opportunities.

James, Judith A

Rheumatic diseases clinics of North America

2014 Volume 40, Issue 3, Page(s) 413–32, vii

Abstract: In recent years, genome-wide association studies have led to an expansion in the identification of regions containing confirmed genetic risk variants within complex human diseases, such as systemic lupus erythematosus (SLE). Many of the strongest SLE ... ...

Abstract	In recent years, genome-wide association studies have led to an expansion in the identification of regions containing confirmed genetic risk variants within complex human diseases, such as systemic lupus erythematosus (SLE). Many of the strongest SLE genetic associations can be divided into groups based on their potential roles in different processes implicated in lupus pathogenesis, including ubiquitination, DNA degradation, innate immunity, cellular immunity, lymphocyte development, and antigen presentation. Recent advances have also shown several genetic associations with SLE subphenotypes and subcriteria. Many areas for further exploration remain to move lupus genetic studies toward clinically informative end points.
MeSH term(s)	Genetic Association Studies ; Genetic Predisposition to Disease ; Genetic Variation ; Humans ; Immunity/genetics ; Lupus Erythematosus, Systemic/complications ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/physiopathology ; Ubiquitination/genetics
Language	English
Publishing date	2014-06-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	92118-x
ISSN	1558-3163 ; 0889-857X
ISSN (online)	1558-3163
ISSN	0889-857X
DOI	10.1016/j.rdc.2014.04.002
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Article ; Online: A High Prevalence of Anti-EBNA1 Heteroantibodies in Systemic Lupus Erythematosus (SLE) Supports Anti-EBNA1 as an Origin for SLE Autoantibodies.

Laurynenka, Viktoryia / Ding, Lili / Kaufman, Kenneth M / James, Judith A / Harley, John B

Frontiers in immunology

2022 Volume 13, Page(s) 830993

Abstract: Background: That Epstein-Barr virus (EBV) infection is associated with systemic lupus erythematosus (SLE) is established. The challenge is to explain mechanistic roles EBV has in SLE pathogenesis. Previous studies identify four examples of autoantibody ... ...

Abstract	Background: That Epstein-Barr virus (EBV) infection is associated with systemic lupus erythematosus (SLE) is established. The challenge is to explain mechanistic roles EBV has in SLE pathogenesis. Previous studies identify four examples of autoantibody cross-reactions between SLE autoantigens and Epstein-Barr nuclear antigen 1 (EBNA1). For two of these examples, the earliest detected autoantibody specifically cross-reacts with EBNA1; thereby, defined EBNA1 epitopes induce a robust autoantibody response in animals. These results suggest that the autoantibodies initiating the process leading to SLE may emerge from the anti-EBNA1 heteroimmune response. If this hypothesis is true, then anti-EBNA1 responses would be more frequent in EBV-infected SLE patients than in EBV-infected controls. We tested this prediction. Methods: We evaluated published East Asian data by selecting those with a positive anti-viral capsid antigen (VCA) antibody immunoglobulin G (IgG) test and determining whether anti-EBNA1 was more common among the EBV-infected SLE cases than among matched EBV-infected controls with conditional logistic regression analysis. Results: All the qualifying SLE patients (100%) in this dataset were EBV-infected compared to age- and sex-matched controls (92.2%) [odds ratio (OR) = 28.6, 95% CI 6.4-∞, p = 8.83 × 10 Conclusions: The association of EBV infection with SLE is reconfirmed. The prediction that anti-EBNA1 is more frequent in these SLE cases than in EBV-infected controls is true, consistent with the hypothesis that anti-EBNA1 contributes to SLE. This second EBV-dependent risk factor is consistent with a molecular mimicry model for the generation of SLE, starting with EBV infection, progressing to anti-EBNA1 response; then molecular mimicry leads to anti-EBNA1 antibodies cross-reacting with an SLE autoantigen, causing autoantibody epitope spreading, and culminating in clinical SLE. These results support the anti-EBNA1 heteroimmune response being a foundation from which pathogenic SLE autoimmunity emerges.
MeSH term(s)	Animals ; Antibodies, Heterophile ; Antibodies, Viral ; Autoantibodies ; Autoantigens ; Capsid Proteins ; Epitopes ; Epstein-Barr Virus Infections ; Epstein-Barr Virus Nuclear Antigens ; Herpesvirus 4, Human ; Humans ; Immunoglobulin G ; Lupus Erythematosus, Systemic ; Prevalence
Chemical Substances	Antibodies, Heterophile ; Antibodies, Viral ; Autoantibodies ; Autoantigens ; Capsid Proteins ; Epitopes ; Epstein-Barr Virus Nuclear Antigens ; Immunoglobulin G ; EBV-encoded nuclear antigen 1 (O5GA75RST7)
Language	English
Publishing date	2022-02-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.830993
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Article ; Online: Hydrogen-Deuterium Exchange Mass Spectrometry Reveals a Novel Binding Region of a Neutralizing Fully Human Monoclonal Antibody to Anthrax Protective Antigen.

Fang, Mulin / Wang, Zhe / Norris, Kathleen / James, Judith A / Wu, Si / Smith, Kenneth

Toxins

2022 Volume 14, Issue 2

Abstract: Anthrax vaccine adsorbed (AVA) containing protective antigen (PA) is the only FDA-approved anthrax vaccine in the United States. Characterization of the binding of AVA-induced anti-PA human antibodies against the PA antigen after vaccination is crucial ... ...

Abstract	Anthrax vaccine adsorbed (AVA) containing protective antigen (PA) is the only FDA-approved anthrax vaccine in the United States. Characterization of the binding of AVA-induced anti-PA human antibodies against the PA antigen after vaccination is crucial to understanding mechanisms of the AVA-elicited humoral immune response. Hydrogen deuterium exchange mass spectrometry (HDX-MS) is often coupled with a short liquid chromatography gradient (e.g., 5-10 min) for the characterization of protein interactions. We recently developed a long-gradient (e.g., 90 min), sub-zero temperature, ultra-high performance liquid chromatography HDX-MS (UPLC-HDX-MS) platform that has significantly increased separation power and limited back-exchange for the analysis of protein samples with high complexity. In this study, we demonstrated the utility of this platform for mapping antibody-antigen epitopes by examining four fully human monoclonal antibodies to anthrax PA. Antibody p1C03, with limited neutralizing activity in vivo, bound to a region on domain 1A of PA. p6C04 and p1A06, with no neutralizing activities, bound to the same helix on domain 3 to prevent oligomerization of PA. We found p6C01 strongly bound to domain 3 on a different helix region. We also identified a secondary epitope for p6C01, which likely leads to the blocking of furin cleavage of PA after p6C01 binding. This novel binding of p6C01 results in highly neutralizing activity. This is the first report of this distinct binding mechanism for a highly neutralizing fully human antibody to anthrax protective antigen. Studying such epitopes can facilitate the development of novel therapeutics against anthrax.
MeSH term(s)	Antibodies, Monoclonal/chemistry ; Antibodies, Monoclonal/immunology ; Antibodies, Neutralizing/chemistry ; Antibodies, Neutralizing/immunology ; Antigens, Bacterial/immunology ; Bacterial Toxins/immunology ; Epitope Mapping ; Epitopes/immunology ; Humans ; Hydrogen Deuterium Exchange-Mass Spectrometry
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Neutralizing ; Antigens, Bacterial ; Bacterial Toxins ; Epitopes ; anthrax toxin
Language	English
Publishing date	2022-01-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2518395-3
ISSN	2072-6651 ; 2072-6651
ISSN (online)	2072-6651
ISSN	2072-6651
DOI	10.3390/toxins14020092
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Article: Gram-Positive Bacteria Cell Wall Peptidoglycan Polymers Activate Human Dendritic Cells to Produce IL-23 and IL-1β and Promote T

Turner, Sean / Raisley, Brent / Roach, Kimberly / Bajaña, Sandra / Munroe, Melissa E / James, Judith A / Coggeshall, K Mark / Kovats, Susan

Microorganisms

2023 Volume 11, Issue 1

Abstract: Gram-positive bacterial infections are a major cause of organ failure and mortality in sepsis. Cell wall peptidoglycan (PGN) is shed during bacterial replication, ... ...

Abstract	Gram-positive bacterial infections are a major cause of organ failure and mortality in sepsis. Cell wall peptidoglycan (PGN) is shed during bacterial replication, and
Language	English
Publishing date	2023-01-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms11010173
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Article ; Online: Biomarkers in connective tissue diseases.

Jog, Neelakshi R / James, Judith A

The Journal of allergy and clinical immunology

2017 Volume 140, Issue 6, Page(s) 1473–1483

Abstract: Autoimmune connective tissue diseases are clinically variable, making biomarkers desirable for assessing future disease risk, supporting early and accurate diagnosis, monitoring disease activity and progression, selecting therapeutics, and assessing ... ...

Abstract	Autoimmune connective tissue diseases are clinically variable, making biomarkers desirable for assessing future disease risk, supporting early and accurate diagnosis, monitoring disease activity and progression, selecting therapeutics, and assessing treatment response. Because of their correlations with specific clinical characteristics and often with disease progression, autoantibodies and other soluble mediators are considered potential biomarkers. Additional biomarkers might reflect downstream pathologic processes or appear because of ongoing inflammation and damage. Because of overlap between diseases, some biomarkers have limited specificity for a single autoimmune connective tissue disease. This review describes select current biomarkers that aid in the diagnosis and treatment of several major systemic autoimmune connective tissue disorders: systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, and anti-neutrophil cytoplasmic antibody-associated vasculitides. Newly proposed biomarkers that target various stages in disease onset or progression are also discussed. Newer approaches to overcome the diversity observed in patients with these diseases and to facilitate personalized disease monitoring and treatment are also addressed.
MeSH term(s)	Animals ; Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/diagnosis ; Arthritis, Rheumatoid/diagnosis ; Autoantibodies/metabolism ; Biomarkers/metabolism ; Connective Tissue Diseases/diagnosis ; Humans ; Lupus Erythematosus, Systemic/diagnosis ; Precision Medicine ; Scleroderma, Systemic/diagnosis
Chemical Substances	Autoantibodies ; Biomarkers
Language	English
Publishing date	2017-12-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2017.10.003
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Article ; Online: Peptidoglycan from Bacillus anthracis Inhibits Human Macrophage Efferocytosis in Part by Reducing Cell Surface Expression of MERTK and TIM-3.

Mytych, Joshua S / Pan, Zijian / Lopez-Davis, Charmaine / Redinger, Nancy / Lawrence, Christina / Ziegler, Jadith / Popescu, Narcis I / James, Judith A / Farris, A Darise

ImmunoHorizons

2024 Volume 8, Issue 3, Page(s) 269–280

Abstract: Bacillus anthracis peptidoglycan (PGN) is a major component of the bacterial cell wall and a key pathogen-associated molecular pattern contributing to anthrax pathology, including organ dysfunction and coagulopathy. Increases in apoptotic leukocytes are ... ...

Abstract	Bacillus anthracis peptidoglycan (PGN) is a major component of the bacterial cell wall and a key pathogen-associated molecular pattern contributing to anthrax pathology, including organ dysfunction and coagulopathy. Increases in apoptotic leukocytes are a late-stage feature of anthrax and sepsis, suggesting there is a defect in apoptotic clearance. In this study, we tested the hypothesis that B. anthracis PGN inhibits the capacity of human monocyte-derived macrophages (MΦ) to efferocytose apoptotic cells. Exposure of CD163+CD206+ MΦ to PGN for 24 h impaired efferocytosis in a manner dependent on human serum opsonins but independent of complement component C3. PGN treatment reduced cell surface expression of the proefferocytic signaling receptors MERTK, TYRO3, AXL, integrin αVβ5, CD36, and TIM-3, whereas TIM-1, αVβ3, CD300b, CD300f, STABILIN-1, and STABILIN-2 were unaffected. ADAM17 is a major membrane-bound protease implicated in mediating efferocytotic receptor cleavage. We found multiple ADAM17-mediated substrates increased in PGN-treated supernatant, suggesting involvement of membrane-bound proteases. ADAM17 inhibitors TAPI-0 and Marimastat prevented TNF release, indicating effective protease inhibition, and modestly increased cell-surface levels of MerTK and TIM-3 but only partially restored efferocytic capacity by PGN-treated MΦ. We conclude that human serum factors are required for optimal recognition of PGN by human MΦ and that B. anthracis PGN inhibits efferocytosis in part by reducing cell surface expression of MERTK and TIM-3.
MeSH term(s)	Humans ; c-Mer Tyrosine Kinase/metabolism ; Bacillus anthracis ; Peptidoglycan/pharmacology ; Peptidoglycan/metabolism ; Anthrax/metabolism ; Anthrax/pathology ; Efferocytosis ; Hepatitis A Virus Cellular Receptor 2/metabolism ; Macrophages/metabolism ; Cell Wall/metabolism ; Cell Wall/pathology
Chemical Substances	c-Mer Tyrosine Kinase (EC 2.7.10.1) ; Peptidoglycan ; Hepatitis A Virus Cellular Receptor 2 ; MERTK protein, human (EC 2.7.10.1)
Language	English
Publishing date	2024-03-22
Publishing country	United States
Document type	Journal Article
ISSN	2573-7732
ISSN (online)	2573-7732
DOI	10.4049/immunohorizons.2300109
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