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Article ; Online: Disease activity drives divergent epigenetic and transcriptomic reprogramming of monocyte subpopulations in systemic lupus erythematosus.

Ferreté-Bonastre, Anna Guiomar / Martínez-Gallo, Mónica / Morante-Palacios, Octavio / Calvillo, Celia Lourdes / Calafell-Segura, Josep / Rodríguez-Ubreva, Javier / Esteller, Manel / Cortés-Hernández, Josefina / Ballestar, Esteban

Annals of the rheumatic diseases

2024

Abstract: Objectives: Systemic lupus erythematosus (SLE) is characterised by systemic inflammation involving various immune cell types. Monocytes, pivotal in promoting and regulating inflammation in SLE, differentiate from classic monocytes into intermediate and ... ...

Abstract	Objectives: Systemic lupus erythematosus (SLE) is characterised by systemic inflammation involving various immune cell types. Monocytes, pivotal in promoting and regulating inflammation in SLE, differentiate from classic monocytes into intermediate and non-classic monocytes, assuming diverse roles and changing their proportions in inflammation. In this study, we investigated the epigenetic and transcriptomic profiles of these and novel monocyte subsets in SLE in relation to activity and progression. Methods: We obtained the DNA methylomes and transcriptomes of classic, intermediate, non-classic monocytes in patients with SLE (at first and follow-up visits) and healthy donors. We integrated these data with single-cell transcriptomics of SLE and healthy donors and interrogated their relationships with activity and progression. Results: In addition to shared DNA methylation and transcriptomic alterations associated with a strong interferon signature, we identified monocyte subset-specific alterations, especially in DNA methylation, which reflect an impact of SLE on monocyte differentiation. SLE classic monocytes exhibited a proinflammatory profile and were primed for macrophage differentiation. SLE non-classic monocytes displayed a T cell differentiation-related phenotype, with Th17-regulating features. Changes in monocyte proportions, DNA methylation and expression occurred in relation to disease activity and involved the STAT pathway. Integration of bulk with single-cell RNA sequencing datasets revealed disease activity-dependent expansion of SLE-specific monocyte subsets, further supported the interferon signature for classic monocytes, and associated intermediate and non-classic populations with exacerbated complement activation. Conclusions: Disease activity in SLE drives a subversion of the epigenome and transcriptome programme in monocyte differentiation, impacting the function of different subsets and allowing to generate predictive methods for activity and progression.
Language	English
Publishing date	2024-02-27
Publishing country	England
Document type	Journal Article
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/ard-2023-225433
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Article ; Online: Utility of lymphocyte phenotype profile to differentiate primary Sjögren's syndrome from sicca syndrome.

Loureiro-Amigo, José / Palacio-García, Carlos / Martínez-Gallo, Mónica / Martínez-Valle, Fernando / Ramentol-Sintas, Marc / Soláns-Laqué, Roser

Rheumatology (Oxford, England)

2021 Volume 60, Issue 12, Page(s) 5647–5658

Abstract: Objective: To assess the potential diagnostic utility of advanced lymphocyte profiling to differentiate between primary Sjögren's Syndrome (pSS) and non-Sjögren Sicca syndrome.: Methods: Distribution of peripheral lymphocyte subpopulations was ... ...

Abstract	Objective: To assess the potential diagnostic utility of advanced lymphocyte profiling to differentiate between primary Sjögren's Syndrome (pSS) and non-Sjögren Sicca syndrome. Methods: Distribution of peripheral lymphocyte subpopulations was analysed by flow cytometry in 68 patients with pSS, 26 patients with sicca syndrome and 23 healthy controls. The ability to discriminate between pSS and sicca syndrome was analysed using the area under the curve (AUC) of the receiver operating characteristic curve of the different lymphocyte subsets. Results: The ratio between naïve/memory B cell proportions showed an AUC of 0.742 to differentiate pSS and sicca syndrome, with a sensitivity of 76.6% and a specificity of 72% for a cut-off value of 3.4. The ratio of non-switched memory B cells to activated CD4+ T cells percentage (BNSM/CD4ACT) presented the highest AUC (0.840) with a sensitivity of 83.3% and specificity of 81.7% for a cut-off value <4.1. To differentiate seronegative pSS patients from sicca patients, the BNSM/CD4ACT ratio exhibited an AUC of 0.742 (sensitivity 75%, specificity 66.7%, cut-off value <4.4), and the number of naïve CD4 T cells had an AUC of 0.821 (sensitivity 76.9%, specificity 88.9%, cut-off value <312/mm3). Conclusion: Patients with pSS show a profound imbalance in the distribution of circulating T and B lymphocyte subsets. The ratio BNSM/CD4ACT is useful to discriminate between pSS and sicca syndrome.
MeSH term(s)	Adult ; Aged ; Diagnosis, Differential ; Female ; Flow Cytometry ; Follow-Up Studies ; Humans ; Keratoconjunctivitis Sicca/diagnosis ; Keratoconjunctivitis Sicca/immunology ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/pathology ; Male ; Middle Aged ; ROC Curve ; Retrospective Studies ; Sjogren's Syndrome/diagnosis ; Sjogren's Syndrome/immunology
Language	English
Publishing date	2021-02-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1464822-2
ISSN	1462-0332 ; 1462-0324
ISSN (online)	1462-0332
ISSN	1462-0324
DOI	10.1093/rheumatology/keab170
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Zs.MO 497: Show issues

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Article ; Online: An algorithm based on immunotherapy discontinuation and liver biopsy spares corticosteroids in two thirds of cases of severe checkpoint inhibitor-induced liver injury.

Riveiro-Barciela, Mar / Barreira-Díaz, Ana / Salcedo, María-Teresa / Callejo-Pérez, Ana / Muñoz-Couselo, Eva / Iranzo, Patricia / Ortiz-Velez, Carolina / Cedrés, Susana / Díaz-Mejía, Nely / Ruiz-Cobo, Juan Carlos / Morales, Rafael / Aguilar-Company, Juan / Zamora, Ester / Oliveira, Mafalda / Sanz-Martínez, María-Teresa / Viladomiu, Lluis / Martínez-Gallo, Mónica / Felip, Enriqueta / Buti, María

Alimentary pharmacology & therapeutics

2024 Volume 59, Issue 7, Page(s) 865–876

Abstract: Background: There are few data on corticosteroids (CS)-sparing strategies for checkpoint inhibitor (ICI)-induced liver injury (ChILI).: Aim: We aimed to assess the performance of a 2-step algorithm for severe ChILI, based on ICI temporary ... ...

Abstract	Background: There are few data on corticosteroids (CS)-sparing strategies for checkpoint inhibitor (ICI)-induced liver injury (ChILI). Aim: We aimed to assess the performance of a 2-step algorithm for severe ChILI, based on ICI temporary discontinuation (step-1) and, if lack of biochemical improvement, CS based on the degree of necroinflammation at biopsy (step-2). Methods: Prospective study that included all subjects with grade 3/4 ChILI. Peripheral extended immunophenotyping was performed. Indication for CS: severe necroinflammation; mild or moderate necroinflammation with later biochemical worsening. Results: From 111 subjects with increased transaminases (January 2020 to August 2023), 44 were diagnosed with grade 3 (N = 35) or grade 4 (N = 9) ChILI. Main reason for exclusion was alternative diagnosis. Lung cancer (13) and melanoma (12) were the most common malignancies. ICI: 23(52.3%) anti-PD1, 8(18.2%) anti-PD-L1, 3(6.8%) anti-CTLA-4, 10(22.7%) combined ICI. Liver injury pattern: hepatocellular (23,52.3%) mixed (12,27.3%) and cholestatic (9,20.5%). 14(32%) presented bilirubin >1.2 mg/dL. Overall, 30(68.2%) patients did not require CS: 22(50.0%) due to ICI discontinuation (step-1) and 8/22 (36.4%) based on the degree of necroinflammation (step-2). Biopsy mainly impacted on grade 3 ChILI, sparing CS in 8 out of 15 (53.3%) non-improvement patients after ICI discontinuation. CD8 Conclusions: An algorithm based on temporary immunotherapy discontinuation and biopsy allows CS avoidance in two thirds of cases of severe ChILI.
MeSH term(s)	Humans ; Prospective Studies ; Chemical and Drug Induced Liver Injury, Chronic ; Adrenal Cortex Hormones/adverse effects ; Immunotherapy/adverse effects ; Biopsy ; Transaminases
Chemical Substances	Adrenal Cortex Hormones ; Transaminases (EC 2.6.1.-)
Language	English
Publishing date	2024-02-07
Publishing country	England
Document type	Journal Article
ZDB-ID	639012-2
ISSN	1365-2036 ; 0269-2813 ; 0953-0673
ISSN (online)	1365-2036
ISSN	0269-2813 ; 0953-0673
DOI	10.1111/apt.17898
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Article ; Online: Role of Skewed X-Chromosome Inactivation in Common Variable Immunodeficiency.

Garcia-Prat, Marina / Batlle-Masó, Laura / Parra-Martínez, Alba / Franco-Jarava, Clara / Martinez-Gallo, Mónica / Aguiló-Cucurull, Aina / Perurena-Prieto, Janire / Castells, Neus / Urban, Blanca / Dieli-Crimi, Romina / Soler-Palacín, Pere / Colobran, Roger

Journal of clinical immunology

2024 Volume 44, Issue 2, Page(s) 54

Abstract: The term common variable immunodeficiency (CVID) encompasses a clinically diverse group of disorders, mainly characterized by hypogammaglobulinemia, insufficient specific antibody production, and recurrent infections. The genetics of CVID is complex, and ...

Abstract	The term common variable immunodeficiency (CVID) encompasses a clinically diverse group of disorders, mainly characterized by hypogammaglobulinemia, insufficient specific antibody production, and recurrent infections. The genetics of CVID is complex, and monogenic defects account for only a portion of cases, typically <30%. Other proposed mechanisms include digenic, oligogenic, or polygenic inheritance and epigenetic dysregulation. In this study, we aimed to assess the role of skewed X-chromosome inactivation (XCI) in CVID. Within our cohort of 131 genetically analyzed CVID patients, we selected female patients with rare variants in CVID-associated genes located on the X-chromosome. Four patients harboring heterozygous variants in BTK (n = 2), CD40LG (n = 1), and IKBKG (n = 1) were included in the study. We assessed XCI status using the HUMARA assay and an NGS-based method to quantify the expression of the 2 alleles in mRNA. Three of the 4 patients (75%) exhibited skewed XCI, and the mutated allele was predominantly expressed in all cases. Patient 1 harbored a hypomorphic variant in BTK (p.Tyr418His), patient 3 had a pathogenic variant in CD40LG (c.288+1G>A), and patient 4 had a hypomorphic variant in IKBKG (p.Glu57Lys) and a heterozygous splice variant in TNFRSF13B (TACI) (c.61+2T>A). Overall, the analysis of our cohort suggests that CVID in a small proportion of females (1.6% in our cohort) is caused by skewed XCI and highly penetrant gene variants on the X-chromosome. Additionally, skewed XCI may contribute to polygenic effects (3.3% in our cohort). These results indicate that skewed XCI may represent another piece in the complex puzzle of CVID genetics.
MeSH term(s)	Humans ; Female ; Common Variable Immunodeficiency ; Alleles ; Agammaglobulinemia ; Antibodies ; CD40 Ligand ; Chromosomes ; I-kappa B Kinase
Chemical Substances	Antibodies ; CD40 Ligand (147205-72-9) ; IKBKG protein, human ; I-kappa B Kinase (EC 2.7.11.10)
Language	English
Publishing date	2024-01-24
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-024-01659-z
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Article ; Online: Thyroid cells from normal and autoimmune thyroid glands suppress T lymphocytes proliferation upon contact revealing a new regulatory inhibitory type of interaction independent of PD1/PDL1.

Álvarez-Sierra, Daniel / Sánchez-Gaona, Nerea / Cruz Cobo, María / Escriche, Alba / Abad, María / Gómez-Brey, Aroa / Bello, Irene / Caubet, Enric / González, Óscar / Zafón, Carles / Iglesias, Carmela / Moreno, Pablo / Petit, Anna / Fernández-Sanmartín, Marco Antonio / Martínez-Gallo, Mónica / Pujol-Borrell, Ricardo

Journal of autoimmunity

2023 Volume 136, Page(s) 103013

Abstract: Immune Checkpoint Receptors include a number of inhibitory receptors that limit tissue damage during immune responses; blocking PD-1/PD-L1 checkpoint receptor axis led to a paradigm shift in cancer immunotherapy but also to autoimmune adverse effects, ... ...

Abstract	Immune Checkpoint Receptors include a number of inhibitory receptors that limit tissue damage during immune responses; blocking PD-1/PD-L1 checkpoint receptor axis led to a paradigm shift in cancer immunotherapy but also to autoimmune adverse effects, prominently thyroid autoimmunity. Although PD-L1 is known to be expressed on thyroid follicular cells (TFCs) of autoimmune glands the role on PD-1/PD-L1 in the interaction between T cells and thyroid cells in the tissue has not been investigated. Here we report that autologous primary TFCs, but not transformed TFCs, inhibit CD4 and CD8 T cell proliferation but no cytokine production. This effect is not, however, mediated by PD-1/PD-L1 nor locally produced cytokines. Beta galactosidase analysis excluded culture-induced senescence as an explanation. High resolution flow cytometry demonstrated that autologous TFC/T cells co-culture induced the expansion of several clusters of double negative (DN) T cells characterized by high expression of activation markers and negative immune checkpoints. Single cell transcriptomic profiling demonstrated that dissociated TFC express numerous candidate molecules for mediating this suppressive activity, including CD40, E-Cadherin and TIGIT ligands. These ligands directly or through the generation of a suppressor population of DN T cells, and not the PD-1/PD-L1 axis, are most likely the responsible of TFC immunosuppressive activity. These results contribute to reveal the complex network of inhibitory mechanism that operate at the tissue level to restrain autoimmunity but also point to pathways, other that PD-1/PD-L1, that can contribute to tumor evasion.
MeSH term(s)	Thyroid Gland ; B7-H1 Antigen/metabolism ; Programmed Cell Death 1 Receptor/metabolism ; CD8-Positive T-Lymphocytes ; Cell Proliferation
Chemical Substances	B7-H1 Antigen ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2023-02-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2023.103013
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Article ; Online: Molecular Challenges in the Diagnosis of X-Linked Chronic Granulomatous Disease: CNVs, Intronic Variants, Skewed X-Chromosome Inactivation, and Gonosomal Mosaicism.

Batlle-Masó, Laura / Rivière, Jacques G / Franco-Jarava, Clara / Martín-Nalda, Andrea / Garcia-Prat, Marina / Parra-Martínez, Alba / Aguiló-Cucurull, Aina / Castells, Neus / Martinez-Gallo, Mónica / Soler-Palacín, Pere / Colobran, Roger

Journal of clinical immunology

2023 Volume 43, Issue 8, Page(s) 1953–1963

Abstract: Chronic granulomatous disease (CGD) is a prototypical inborn error of immunity affecting phagocytes, in which these cells are unable to produce reactive oxygen species. CGD is caused by defects in genes encoding subunits of the NADPH oxidase enzyme ... ...

Abstract	Chronic granulomatous disease (CGD) is a prototypical inborn error of immunity affecting phagocytes, in which these cells are unable to produce reactive oxygen species. CGD is caused by defects in genes encoding subunits of the NADPH oxidase enzyme complex (CYBA, CYBB, CYBC1, NCF1, NCF2, NCF4); inflammatory responses are dysregulated, and patients are highly susceptible to recurrent severe bacterial and fungal infections. X-linked CGD (XL-CGD), caused by mutations in the CYBB gene, is the most common and severe form of CGD. In this study, we describe the analytical processes undertaken in 3 families affected with XL-CGD to illustrate several molecular challenges in the genetic diagnosis of this condition: in family 1, a girl with a heterozygous deletion of CYBB exon 13 and skewed X-chromosome inactivation (XCI); in family 2, a boy with a hemizygous deletion of CYBB exon 7, defining its consequences at the mRNA level; and in family 3, 2 boys with the same novel intronic variant in CYBB (c.1151 + 6 T > A). The variant affected the splicing process, although a small fraction of wild-type mRNA was produced. Their mother was a heterozygous carrier, while their maternal grandmother was a carrier in form of gonosomal mosaicism. In summary, using a variety of techniques, including an NGS-based targeted gene panel and deep amplicon sequencing, copy number variation calling strategies, microarray-based comparative genomic hybridization, and cDNA analysis to define splicing defects and skewed XCI, we show how to face and solve some uncommon genetic mechanisms in the diagnosis of XL-CGD.
MeSH term(s)	Male ; Female ; Humans ; Mosaicism ; Granulomatous Disease, Chronic/diagnosis ; Granulomatous Disease, Chronic/genetics ; Comparative Genomic Hybridization ; DNA Copy Number Variations ; Mutation/genetics ; RNA, Messenger ; Chromosomes
Chemical Substances	RNA, Messenger
Language	English
Publishing date	2023-08-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-023-01556-x
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Article ; Online: Common Variable Immunodeficiency and Neurodevelopmental Delay Due to a 13Mb Deletion on Chromosome 4 Including the NFKB1 Gene: A Case Report.

Franco-Jarava, Clara / Valenzuela, Irene / Riviere, Jacques G / Garcia-Prat, Marina / Martínez-Gallo, Mónica / Dieli-Crimi, Romina / Castells, Neus / Batlle-Masó, Laura / Soler-Palacin, Pere / Colobran, Roger

Frontiers in immunology

2022 Volume 13, Page(s) 897975

Abstract: Syndromic immunodeficiencies are a heterogeneous group of inborn errors of immunity that can affect the development of non-immune organs and systems. The genetic basis of these immunodeficiencies is highly diverse, ranging from monogenic defects to large ...

Abstract	Syndromic immunodeficiencies are a heterogeneous group of inborn errors of immunity that can affect the development of non-immune organs and systems. The genetic basis of these immunodeficiencies is highly diverse, ranging from monogenic defects to large chromosomal aberrations. Antibody deficiency is the most prevalent immunological abnormality in patients with syndromic immunodeficiencies caused by chromosomal rearrangements, and usually manifests as a common variable immunodeficiency (CVID)-like phenotype. Here we describe a patient with a complex phenotype, including neurodevelopmental delay, dysmorphic features, malformations, and CVID (hypogammaglobulinemia, reduced pre-switch and switch memory B cells, and impaired vaccine response). Microarray-based comparative genomic hybridization (aCGH) revealed a 13-Mb deletion on chromosome 4q22.2-q24 involving 53 genes, some of which were related to the developmental manifestations in our patient. Although initially none of the affected genes could be linked to his CVID phenotype, subsequent reanalysis identified
MeSH term(s)	Agammaglobulinemia ; Chromosome Aberrations ; Chromosome Deletion ; Chromosomes, Human, Pair 4 ; Common Variable Immunodeficiency/genetics ; Comparative Genomic Hybridization ; Humans ; NF-kappa B p50 Subunit ; Primary Immunodeficiency Diseases
Chemical Substances	NF-kappa B p50 Subunit ; NFKB1 protein, human
Language	English
Publishing date	2022-06-17
Publishing country	Switzerland
Document type	Case Reports ; 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.2022.897975
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Article ; Online: Commercialized kits to assess T-cell responses against SARS-CoV-2 S peptides. A pilot study in health care workers.

Martínez-Gallo, Mónica / Esperalba, Juliana / Pujol-Borrell, Ricardo / Sandá, Víctor / Arrese-Muñoz, Iria / Fernández-Naval, Candela / Antón, Andrés / Cardona, Victoria / Labrador-Horrillo, Moisés / Pumarola, Tomás / Hernandéz-González, Manuel

Medicina clinica (English ed.)

2022 Volume 159, Issue 3, Page(s) 116–123

Abstract: Background: It is crucial to assess the levels of protection generated by natural infection or SARS-CoV-2 vaccines, mainly in individuals professionally exposed and in vulnerable groups. Measuring T-cell responses may complement antibody tests currently ...

Abstract	Background: It is crucial to assess the levels of protection generated by natural infection or SARS-CoV-2 vaccines, mainly in individuals professionally exposed and in vulnerable groups. Measuring T-cell responses may complement antibody tests currently in use as correlates of protection. Our aim was to assess the feasibility of a validated assay of T-cell responses. Methods: Twenty health-care-workers (HCW) were included. Antibody test to SARS-CoV-2 N and S-proteins in parallel with a commercially available whole-blood-interferon-gamma-release-assay (IGRA) to S-peptides and two detection methods, CLIA and ELISA were determined. Results: IGRA test detected T-cell responses in naturally exposed and vaccinated HCW already after first vaccination dose. The correlation by the two detection methods was very high ( Conclusion: Whole-blood-IGRA-tests amenable to automation and constitutes a promising additional tool for measuring the state of the immune response to SARS-CoV-2; they are applicable to large number of samples and may become a valuable correlate of protection to COVID-19, particularly for vulnerable groups at risk of being re-exposed to infection, as are health-care-workers.
Language	English
Publishing date	2022-08-19
Publishing country	Spain
Document type	Journal Article
ISSN	2387-0206
ISSN (online)	2387-0206
DOI	10.1016/j.medcle.2021.09.028
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Article ; Online: Activation of the Monocyte/Macrophage System and Abnormal Blood Levels of Lymphocyte Subpopulations in Individuals with Autism Spectrum Disorder: A Systematic Review and Meta-Analysis.

Arteaga-Henríquez, Gara / Lugo-Marín, Jorge / Gisbert, Laura / Setién-Ramos, Imanol / Martínez-Gallo, Mónica / Pujol-Borrell, Ricardo / Ramos-Quiroga, Josep Antoni

International journal of molecular sciences

2022 Volume 23, Issue 22

Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental condition with a so far unknown etiology. Increasing evidence suggests that a state of systemic low-grade inflammation may be involved in the pathophysiology of this condition. However, studies ... ...

Abstract	Autism spectrum disorder (ASD) is a neurodevelopmental condition with a so far unknown etiology. Increasing evidence suggests that a state of systemic low-grade inflammation may be involved in the pathophysiology of this condition. However, studies investigating peripheral blood levels of immune cells, and/or of immune cell activation markers such as neopterin are lacking and have provided mixed findings. We performed a systematic review and meta-analysis of studies comparing total and differential white blood cell (WBC) counts, blood levels of lymphocyte subpopulations and of neopterin between individuals with ASD and typically developing (TD) controls (PROSPERO registration number: CRD CRD42019146472). Online searches covered publications from 1 January 1994 until 1 March 2022. Out of 1170 publication records identified, 25 studies were finally included. Random-effects meta-analyses were carried out, and sensitivity analyses were performed to control for potential moderators. Results: Individuals with ASD showed a significantly higher WBC count (k = 10, g = 0.29, p = 0.001, I2 = 34%), significantly higher levels of neutrophils (k = 6, g = 0.29, p = 0.005, I2 = 31%), monocytes (k = 11, g = 0.35, p < 0.001, I2 = 54%), NK cells (k = 7, g = 0.36, p = 0.037, I2 = 67%), Tc cells (k = 4, g = 0.73, p = 0.021, I2 = 82%), and a significantly lower Th/Tc cells ratio (k = 3, g = −0.42, p = 0.008, I2 = 0%), compared to TD controls. Subjects with ASD were also characterized by a significantly higher neutrophil-to-lymphocyte ratio (NLR) (k = 4, g = 0.69, p = 0.040, I2 = 90%), and significantly higher neopterin levels (k = 3, g = 1.16, p = 0.001, I2 = 97%) compared to TD controls. No significant differences were found with respect to the levels of lymphocytes, B cells, Th cells, Treg cells, and Th17 cells. Sensitivity analysis suggested that the findings for monocyte and neutrophil levels were robust, and independent of other factors, such as medication status, diagnostic criteria applied, and/or the difference in age or sex between subjects with ASD and TD controls. Taken together, our findings suggest the existence of a chronically (and systemically) activated inflammatory response system in, at least, a subgroup of individuals with ASD. This might have not only diagnostic, but also, therapeutic implications. However, larger longitudinal studies including more homogeneous samples and laboratory assessment methods and recording potential confounding factors such as body mass index, or the presence of comorbid psychiatric and/or medical conditions are urgently needed to confirm the findings.
MeSH term(s)	Humans ; Monocytes ; Autism Spectrum Disorder ; Neopterin ; Leukocytes ; Lymphocyte Subsets ; Th17 Cells ; Macrophages
Chemical Substances	Neopterin (670-65-5)
Language	English
Publishing date	2022-11-18
Publishing country	Switzerland
Document type	Meta-Analysis ; Systematic Review ; Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232214329
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Article ; Online: Detection and evolutionary dynamics of somatic FAS variants in autoimmune lymphoproliferative syndrome: Diagnostic implications.

Batlle-Masó, Laura / Garcia-Prat, Marina / Parra-Martínez, Alba / Franco-Jarava, Clara / Aguiló-Cucurull, Aina / Velasco, Pablo / Antolín, María / Rivière, Jacques G / Martín-Nalda, Andrea / Soler-Palacín, Pere / Martínez-Gallo, Mónica / Colobran, Roger

Frontiers in immunology

2022 Volume 13, Page(s) 1014984

Abstract: Autoimmune lymphoproliferative syndrome (ALPS) is a rare primary immune disorder characterized by impaired apoptotic homeostasis. The clinical characteristics include lymphoproliferation, autoimmunity (mainly cytopenia), and an increased risk of lymphoma. ...

Abstract	Autoimmune lymphoproliferative syndrome (ALPS) is a rare primary immune disorder characterized by impaired apoptotic homeostasis. The clinical characteristics include lymphoproliferation, autoimmunity (mainly cytopenia), and an increased risk of lymphoma. A distinctive biological feature is accumulation (>2.5%) of an abnormal cell subset composed of TCRαβ
MeSH term(s)	Child ; Humans ; Autoimmune Lymphoproliferative Syndrome/diagnosis ; Autoimmune Lymphoproliferative Syndrome/genetics ; Autoimmune Lymphoproliferative Syndrome/therapy ; Brain Neoplasms ; Glioma
Language	English
Publishing date	2022-11-18
Publishing country	Switzerland
Document type	Journal Article ; 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.2022.1014984
Database	MEDical Literature Analysis and Retrieval System OnLINE

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