Association of polymorphisms in the &lt;i&gt;ICOS&lt;/i&gt; and &lt;i&gt;ICOSL&lt;/i&gt; genes with the pathogenesis of autoimmune thyroid diseases

Yoshie, Namiki; Watanabe, Mikio; Inoue, Naohisa; Kawaguchi, Hayaka; Hidaka, Yoh; Iwatani, Yoshinori

doi:10.1507/endocrj.ej15-0435

Cited by 6 publications

(4 citation statements)

References 39 publications

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“…Single cells from spleens and draining lymph nodes of WT skin-grafted Dsg3 -/mice and from spleens of Rag1 -/mice given the various cell populations from WT skin-grafted Dsg3 -/mice were surface-stained at 48C for 20 minutes with the following antibodies: anti-CD3e-BV510 (145-2C11), anti-CD3e-PerCP-Cy5.5 (145-2C11), anti-CD4-APC-Cy7 (GK1.5), anti-CD4-PE-Cy7 (GK1.5), biotin anti-CXCR5 (2G8), anti-CD44-APC-R700 (IM7), anti-CD62L-BB515 (MEL-14), anti-CD19-PE-CF594 (1D3), anti-CD25-BV786 (PC61) anti-B220-BV650 (RA3-6B2), anti-B220-PerCP-Cy5.5 (RA3-6B2), anti-Fas-BV421 (Jo2), anti-Fas-PE-Cy7 (Jo2), anti-GL7-PE (GL7), anti-CD138-APC (281-2), anti-NK1.1-Alexa Fluor 700 (PK136) (all from BD Biosciences); anti-PD-1-BV605 (29F.1A12), anti-PD-1-PE (29F.1A12) (both from BioLegend San Diego, Calif); anti-ICOS-PE-Cy7 (C398.4A), anti-IgD-APC-Cy7 (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26), and anti-CD3-Alexa Fluor 700 (500A2) (all from Invitrogen). For the staining of human PBMCs the following were used for surface staining at 48C for 20 minutes: anti-CD3-BV786 (SK7), anti-CD4-APC-Cy7 (RPA-T4), biotin anti-CXCR5 (RF8B2), anti-CD45RA-FITC (HI100), anti-CCR7-PE-Cy7 (3D12), anti-CD14-BV510 (M4P-9), anti-CD8-BV510 (SK1), anti-CCR6-APC-R700 (11A9) (all from BD Biosciences); anti-PD-1-BV605 (EH12.2H7) (from BioLegend); anti-CD19-BV510 (HIB19), anti-ICOS-APC (ISA-3) (both from Invitrogen); and anti-CXCR3-PE (49801; R&D Systems).…”

Section: Flow Cytometrymentioning

confidence: 99%

“…ICOS can be expressed on all activated T cells, but is especially critical in T FH cell differentiation and maintenance, as well as the GC response. 10,11 ICOS polymorphisms have been associated with various autoimmune diseases, 12,13 and anti-ICOS blocking antibody has been used to target ICOS 1 T FH cell activation in mouse models of autoimmune disease, including systemic lupus erythematosus and lupus nephritis. 14,15 Recently, an anti-ICOS depleting antibody was shown to control systemic sclerosis by reducing ICOS 1 T FH -like cells in the skin.…”

mentioning

confidence: 99%

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Targeting inducible costimulator expressed on CXCR5+PD-1+ TH cells suppresses the progression of pemphigus vulgaris

Kim

Han

Choi

et al. 2020

Journal of Allergy and Clinical Immunology

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Section: Flow Cytometrymentioning

confidence: 99%

mentioning

confidence: 99%

Targeting inducible costimulator expressed on CXCR5+PD-1+ TH cells suppresses the progression of pemphigus vulgaris

Kim

Han

Choi

et al. 2020

Journal of Allergy and Clinical Immunology

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“…ICOSLG-ICOS interaction is implicated in multiple immune processes, such as the establishment of CD8+ tissue resident T cells in intestine ( 64 ). Altogether, these interactions point to the importance of ICOS interactions, which have been found to have relevance in multiple autoimmune diseases ( 65 – 67 ).…”

Section: Discussionmentioning

confidence: 89%

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Pediatric Coeliac Disease Patients Suggests Potential Pre-Seroconversion Markers

et al. 2022

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Celiac Disease (CeD) is a complex immune disorder involving villous atrophy in the small intestine that is triggered by gluten intake. Current CeD diagnosis is based on late-stage pathophysiological parameters such as detection of specific antibodies in blood and histochemical detection of villus atrophy and lymphocyte infiltration in intestinal biopsies. To date, no early onset biomarkers are available that would help prevent widespread villous atrophy and severe symptoms and co-morbidities. To search for novel CeD biomarkers, we used single-cell RNA sequencing (scRNAseq) to investigate PBMC samples from 11 children before and after seroconversion for CeD and 10 control individuals matched for age, sex and HLA-genotype. We generated scRNAseq profiles of 9559 cells and identified the expected major cellular lineages. Cell proportions remained stable across the different timepoints and health conditions, but we observed differences in gene expression profiles in specific cell types when comparing patient samples before and after disease development and comparing patients with controls. Based on the time when transcripts were differentially expressed, we could classify the deregulated genes as biomarkers for active CeD or as potential pre-diagnostic markers. Pathway analysis showed that active CeD biomarkers display a transcriptional profile associated with antigen activation in CD4+ T cells, whereas NK cells express a subset of biomarker genes even before CeD diagnosis. Intersection of biomarker genes with CeD-associated genetic risk loci pinpointed genetic factors that might play a role in CeD onset. Investigation of potential cellular interaction pathways of PBMC cell subpopulations highlighted the importance of TNF pathways in CeD. Altogether, our results pinpoint genes and pathways that are altered prior to and during CeD onset, thereby identifying novel potential biomarkers for CeD diagnosis in blood.

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“…Therefore, ICOSL may be an option for the treatment of autoimmune diseases. Studies have shown that the polymorphisms of ICOSLG were associated with an increased risk of RA, autoimmune thyroid diseases, and SLE (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

The susceptibility of single nucleotide polymorphisms located within co-stimulatory pathways to systemic lupus erythematosus

Chen,

Lin,

Hsu

et al. 2024

Front. Immunol.

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IntroductionAutoimmune diseases result from the loss of immune tolerance, and they exhibit complex pathogenic mechanisms that remain challenging to effectively treat. It has been reported that the altered expression levels of co-stimulatory/inhibitory molecules will affect the level of T/B cell activation and lead to the loss of immune tolerance.MethodsIn this study, we evaluated the gene polymorphisms of the ligand genes corresponding co-stimulatory system that were expressed on antigen-presenting cells (CD80, CD86, ICOSLG, and PDL1) from 60 systemic lupus erythematosus (SLE) patients and 60 healthy controls.ResultsThe results showed that rs16829984 and rs57271503 of the CD80 gene and rs4143815 of the PDL1 gene were associated with SLE, in which the G-allele of rs16829984 (p=0.022), the A-allele of rs57271503 (p=0.029), and the GG and GC genotype of rs4143815 (p=0.039) may be risk polymorphisms for SLE.DiscussionThese SNPs are in the promoter and 3’UTR of the genes, so they may affect the transcription and translation activity of the genes, thereby regulating immune function and contributing to the development of SLE.

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Association of polymorphisms in the <i>ICOS</i> and <i>ICOSL</i> genes with the pathogenesis of autoimmune thyroid diseases

Cited by 6 publications

References 39 publications

Targeting inducible costimulator expressed on CXCR5+PD-1+ TH cells suppresses the progression of pemphigus vulgaris

Targeting inducible costimulator expressed on CXCR5+PD-1+ TH cells suppresses the progression of pemphigus vulgaris

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Pediatric Coeliac Disease Patients Suggests Potential Pre-Seroconversion Markers

The susceptibility of single nucleotide polymorphisms located within co-stimulatory pathways to systemic lupus erythematosus

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