scholarly journals Enhancement of the Soluble Form of OX40 and OX40L Costimulatory Molecules but Reduction of the Membrane Form in Type 1 Diabetes (T1D)

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jingnan An ◽  
Sisi Ding ◽  
Sicheng Li ◽  
Lili Sun ◽  
Xin Chang ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Type 1 Diabetes ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Clinical Characteristics ◽  
Inflammatory Factors ◽  
Soluble Form ◽  
Healthy Control ◽  
First Time

This study analyzed the expression of membrane OX40 and OX40L (mOX40 and mOX40L) and levels of soluble OX40 and OX40L (sOX40 and sOX40L) in T1D patients to determine their clinical significance. Peripheral blood (PB) was collected from patients with T1D and healthy control participants. Expression of mOX40 and mOX40L on immune cells was detected by flow cytometry. Levels of sOX40 and sOX40L in sera were measured by ELISA. We demonstrated for the first time enhanced sOX40 and sOX40L expression and reduced mOX40 and mOX40L levels in T1D patients which correlated with the clinical characteristics and inflammatory factors. These results suggest that OX40/OX40L signal may be promising biomarkers and associated with the pathogenesis of T1D.

scholarly journals A study of 51 subtypes of peripheral blood immune cells in newly diagnosed young type 1 diabetes patients

2019 ◽  
Vol 198 (1) ◽  
pp. 57-70 ◽  
Author(s):  
A. Oras ◽  
A. Peet ◽  
T. Giese ◽  
V. Tillmann ◽  
R. Uibo
Keyword(s):  
Type 1 Diabetes ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Newly Diagnosed ◽  
Diabetes Patients

scholarly journals Phenotypical Changes of Hematopoietic Stem and Progenitor Cells in Sepsis Patients: Correlation With Immune Status?

2021 ◽  
Vol 11 ◽  
Author(s):  
Ping Wang ◽  
Jun Wang ◽  
Yi-hao Li ◽  
Lan Wang ◽  
Hong-cai Shang ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Immune System ◽  
Blood Cell ◽  
Progenitor Cells ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Hematopoietic Stem ◽  
Stem And Progenitor Cells ◽  
Healthy Control ◽  
Kinetics Of

Background: Sepsis is life-threatening organ dysfunction associated with high risk of death. The immune response of sepsis is complex and varies over time. The immune cells are derived from hematopoietic stem and progenitor cells (HSPCs) which can respond to many infections. Our previous study found that sepsis causes HSPC dysregulation in mouse. But few studies have previously investigated the kinetics of HSPC and its contribution to immune system in sepsis patients.Purpose: We aimed to identify the kinetics of HSPCs and their contribution to immune system in sepsis patients.Methods: We enrolled eight sepsis patients and five healthy control subjects. Peripheral blood (PB) samples from each patient were collected three times: on the first, fourth, and seventh days, once from each healthy control subject. Peripheral blood mononuclear cells (PBMCs) were isolated by density centrifugation and stained with cocktails of antibodies. Populations of HSPCs and their subpopulation were analyzed by flow cytometry. Immune cells were characterized by flow cytometry and blood cell analysis. Correlations between HSPCs and immune cells were analyzed using the Pearson correlation test.Results: We found that the frequency of HSPCs (CD34+ cells and CD34+CD38+ cells) in sepsis patients on day 4 was significantly higher than that in the healthy controls. The most pronounced change in subpopulation analysis is the frequency of common myeloid progenitors (CMPs; CD34+CD38+CD135+CD45RA−). But no difference in the immunophenotypically defined hematopoietic stem cells (HSCs; CD34+CD38−CD90+CD45RA−) in sepsis patients was observed due to rare HSC numbers in PB. The number of PBMCs and lymphocytes are decreased, whereas the white blood cell (WBC) and neutrophil counts were increased in sepsis patients. Importantly, we found a negative correlation between CD34+ on day 1 and WBC and lymphocytes on day 4 from correlation analysis in sepsis patients.Conclusion: The present study demonstrated that the HSPC and its subpopulation in sepsis patients expanded. Importantly, the changes in HSPCs at early time points in sepsis patients have negative correlations with later immune cells. Our results may provide a novel diagnostic indicator and a new therapeutic approach.

scholarly journals Identifying Changes in Peripheral Lymphocyte Subpopulations in Adult Onset Type 1 Diabetes

2021 ◽  
Vol 12 ◽  
Author(s):  
Aina Teniente-Serra ◽  
Eduarda Pizarro ◽  
Bibiana Quirant-Sánchez ◽  
Marco A. Fernández ◽  
Marta Vives-Pi ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Type 1 Diabetes ◽  
B Cells ◽  
Peripheral Blood ◽  
Disease Onset ◽  
Lymphocyte Subpopulations ◽  
Effector Memory ◽  
Transitional B Cells

T- and B-lymphocytes play an important role in the pathogenesis of type 1 diabetes (T1D), a chronic disease caused by the autoimmune destruction of the insulin-producing cells in the pancreatic islets. Flow cytometry allows their characterization in peripheral blood, letting to investigate changes in cellular subpopulations that can provide insights in T1D pathophysiology. With this purpose, CD4+ and CD8+ T cells (including naïve, central memory, effector memory and terminally differentiated effector (TEMRA), Th17 and Tregs) and B cells subsets (naïve, unswitched memory, switched memory and transitional B cells) were analysed in peripheral blood of adult T1D patients at disease onset and after ≥2 years using multiparametric flow cytometry. Here we report changes in the percentage of early and late effector memory CD4+ and CD8+ T cells as well as of naïve subsets, regulatory T cells and transitional B cells in peripheral blood of adult patients at onset of T1D when compared with HD. After 2 years follow-up these changes were maintained. Also, we found a decrease in percentage of Th17 and numbers of T cells with baseline. In order to identify potential biomarkers of disease, ROC curves were performed being late EM CD4 T cell subset the most promising candidate. In conclusion, the observed changes in the percentage and/or absolute number of lymphocyte subpopulations of adult T1D patients support the hypothesis that effector cells migrate to the pancreas and this autoimmune process perseveres along the disease. Moreover, multiparametric flow allows to identify those subsets with potential to be considered biomarkers of disease.

scholarly journals Mucosal-associated invariant T cell alterations during the development of human type 1 diabetes

Diabetologia ◽  
2020 ◽  
Vol 63 (11) ◽  
pp. 2396-2409
Author(s):  
Ahmad M. Gazali ◽  
Anna-Mari Schroderus ◽  
Kirsti Näntö-Salonen ◽  
Reeta Rintamäki ◽  
Jussi Pihlajamäki ◽  
...  
Keyword(s):  
T Cells ◽  
Type 1 Diabetes ◽  
Peripheral Blood ◽  
Γδ T Cells ◽  
Newly Diagnosed ◽  
Cross Sectional ◽  
Mait Cells ◽  
Healthy Control ◽  
Cell Alterations

Abstract Aims/hypothesis Mucosal-associated invariant T (MAIT) cells are innate-like T cells that recognise derivatives of bacterial riboflavin metabolites presented by MHC-Ib-related protein 1 (MR1) molecules and are important effector cells for mucosal immunity. Their development can be influenced by the intestinal microbiome. Since the development of type 1 diabetes has been associated with changes in the gut microbiome, this can be hypothesised to lead to alterations in circulating MAIT cells. Accordingly, peripheral blood MAIT cell alterations have been reported previously in patients with type 1 diabetes. However, a comprehensive analysis of the frequency and phenotype of circulating MAIT cells at different stages of type 1 diabetes progression is currently lacking. Methods We analysed the frequency, phenotype and functionality of peripheral blood MAIT cells, as well as γδ T cells, invariant natural killer T (iNKT) cells and natural killer (NK) cells with flow cytometry in a cross-sectional paediatric cohort (aged 2–15) consisting of 51 children with newly diagnosed type 1 diabetes, 27 autoantibody-positive (AAb+) at-risk children, and 113 healthy control children of similar age and HLA class II background. The frequency of MAIT cells was also assessed in a separate cross-sectional adult cohort (aged 19–39) of 33 adults with established type 1 diabetes and 37 healthy individuals of similar age. Results Children with newly diagnosed type 1 diabetes displayed a proportional increase of CD8−CD27− MAIT cells compared with healthy control children (median 4.6% vs 3.1% of MAIT cells, respectively, p = 0.004), which was associated with reduced expression of C-C chemokine receptor (CCR)5 (median 90.0% vs 94.3% of MAIT cells, p = 0.02) and β7 integrin (median 73.5% vs 81.7% of MAIT cells, p = 0.004), as well as decreased production of IFN-γ (median 57.1% vs 69.3% of MAIT cells, p = 0.04) by the MAIT cells. The frequency of MAIT cells was also decreased in AAb+ children who later progressed to type 1 diabetes compared with healthy control children (median 0.44% vs 0.96% of CD3+ T cells, p = 0.04), as well as in adult patients with a short duration of type 1 diabetes (less than 6 years after diagnosis) compared with control individuals (median 0.87% vs 2.19% of CD3+ T cells, p = 0.007). No alterations in γδ T cell, iNKT cell or NK cell frequencies were observed in children with type 1 diabetes or in AAb+ children, with the exception of an increased frequency of IL-17A+ γδ T cells in children with newly diagnosed diabetes compared with healthy control children (median 1.58% vs 1.09% of γδ T cells, p = 0.002). Conclusions/interpretation Changes in the frequency and phenotype of circulating MAIT cells were detectable before, at the onset and after diagnosis of type 1 diabetes in cross-sectional cohorts. Our results suggest a possible temporal association between peripheral blood MAIT cell alterations and the clinical onset of type 1 diabetes.

Biochemical and clinical characteristics of polysystic ovarian syndrome (PCOS) in women with and without type 1 diabetes (TID)

2017 ◽  
Author(s):  
Anjuli Gunness ◽  
Agnieska Pazderska ◽  
Mohamed Ahmed ◽  
Niamh Phelan ◽  
Gerard Boran ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Clinical Characteristics ◽  
Ovarian Syndrome

693-P: Oxidative–Antioxidant Balance after Maximum Intensity Exercise in Men with Type 1 Diabetes Treated with a Personal Insulin Pump vs. Healthy Control

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 693-P
Author(s):  
BARTłOMIEJ MATEJKO ◽  
ŁUKASZ TOTA ◽  
MAłGORZATA MORAWSKA ◽  
SANDRA MROZINSKA ◽  
WANDA PILCH ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Insulin Pump ◽  
Maximum Intensity ◽  
Healthy Control

scholarly journals HLA class I genes modulate disease risk and age at onset together with DR-DQ in Chinese patients with insulin-requiring type 1 diabetes

Diabetologia ◽  
2021 ◽  
Author(s):  
Ziyu Jiang ◽  
Wenqian Ren ◽  
Hua Liang ◽  
Jinhua Yan ◽  
Daizhi Yang ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Disease Risk ◽  
Hla Class I ◽  
Class I ◽  
Chinese Patients ◽  
Onset Age ◽  
Disease Heterogeneity ◽  
Negatively Associated ◽  
Healthy Control

Abstract Aims/hypothesis The study aimed to investigate the effects of HLA class I genes on susceptibility to type 1 diabetes with different onset ages, in addition to the well-established effects of HLA class II genes. Methods A total of 361 patients with type 1 diabetes (192 patients with onset <18 years and 169 patients with onset ≥18 years) and 500 healthy control participants from China were enrolled and genotyped for the HLA-A, -B, -C, -DQA1, -DQB1 and -DRB1 genes using next-generation sequencing. Results The susceptible DR3 (β = −0.09, p = 0.0009) and DR4-DQ8 (β = −0.13, p = 0.0059) haplotypes were negatively associated with onset age, while the protective DR11 (β = 0.21, p = 0.0314) and DR12 (β = 0.27, p < 0.0001) haplotypes were positively associated with onset age. After adjustment for linkage disequilibrium with DR-DQ haplotypes, A*11:01:01 was positively associated with onset age (β = 0.06, p = 0.0370), while the susceptible C*15:02:01 was negatively associated with onset age (β = −0.21, p = 0.0050). The unit for β was double square-root (fourth root) transformed years of change in onset age associated with per copy of the HLA haplotype/allele. In addition, B*46:01:01 was protective (OR 0.41, 0.46; pc [corrected for multiple comparisons] = 0.0044, 0.0040), whereas A*24:02:01 (OR 2.71, 2.25; pc = 0.0003, 0.0002) and B*54:01:01 (OR 3.96, 3.79; pc = 0.0018, 0.0004) were predisposing in both the <18 group and the ≥18 group compared with healthy control participants. In the context of DR4-DQ4, A*11:01:01 (61.29% vs 28.26%, pc = 0.0144) was increased while the predisposing A*24:02:01 (19.35% vs 47.83%, pc = 0.0403) was decreased in patients with onset ≥18 years when compared with patients with onset <18 years. Conclusions/interpretation In addition to DR-DQ haplotypes, novel HLA class I alleles were detected to play a role in susceptibility to type 1 diabetes with different onset ages, which could improve the understanding of disease heterogeneity and has implications for the design of future studies. Graphical abstract

scholarly journals Mouse IgG3 binding to macrophage-like cells is prevented by deglycosylation of the antibody or by Accutase treatment of the cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alicja Karabasz ◽  
Monika Bzowska ◽  
Joanna Bereta ◽  
Maria Czarnek ◽  
Maja Sochalska ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Complex Network ◽  
Immune Cells ◽  
Specific Receptor ◽  
Fcγ Receptors ◽  
Specific Receptors ◽  
First Time

AbstractThe binding of mouse IgG3 to Fcγ receptors (FcγR) and the existence of a mouse IgG3-specific receptor have been discussed for 40 years. Recently, integrin beta-1 (ITGB1) was proposed to be a part of an IgG3 receptor involved in the phagocytosis of IgG3-coated pathogens. We investigated the interaction of mouse IgG3 with macrophage-like J774A.1 and P388D1 cells. The existence of an IgG3-specific receptor was verified using flow cytometry and a rosetting assay, in which erythrocytes clustered around the macrophage-like cells coated with an erythrocyte-specific IgG3. Our findings confirmed that receptors binding antigen-free IgG3 are present on J774A.1 and P388D1 cells. We demonstrated for the first time that the removal of N-glycans from IgG3 completely abolished its binding to the cells. Moreover, we discovered that the cells treated with Accutase did not bind IgG3, indicating that IgG3-specific receptors are substrates of this enzyme. The results of antibody-mediated blocking of putative IgG3 receptors suggested that apart from previously proposed ITGB1, FcγRII, FcγRIII, also additional, still unknown, receptor is involved in IgG3 binding. These findings indicate that there is a complex network of glycan-dependent interactions between mouse IgG3 and the surface of effector immune cells.

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