Evaluation of the role of B7-H3 haplotype in association with impaired B7-H3 expression and protection against type 1 diabetes in Chinese Han population

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Abstract

Background

Type 1 Diabetes (T1D) is a T cell-mediated autoimmune disorder caused by the destruction of insulin-secreting cells. B7-H3 (CD276) plays a vital role in T cell response. However, B7-H3 expression and its clinical significance in T1D remain unclear. The aim of this study was to investigate the correlations between the expression of B7-H3 and clinical parameters in T1D patients. The possible role of B7-H3 gene variants with T1D was also discussed.

Methods

Four B7-H3 single nucleotide polymorphisms (SNPs) were genotyped in 121 T1D patients and 120 healthy controls by polymerase chain reaction (PCR) direct sequencing. Expression of membrane B7-H3 (mB7-H3) in peripheral blood lymphocytes was determined by flow cytometry. Levels of soluble B7-H3 (sB7-H3) in serum were analyzed by enzyme linked immunosorbent assay (ELISA).

Results

The B7-H3 haplotype T-A-C-T was less frequently observed in T1D patients compared to the controls (OR: 0.31, 95% CI: 0.16–0.61). B7-H3 expression on monocytes showed significant upregulation in T1D patients and was positively correlated with several clinical features including ALT, fast C-peptide 120 min, HbAlc, IFN-γ, IL-6 and TNF-α ( P < 0.05). The concentration of sB7-H3 in serum increased in T1D patients (P < 0.0001). We also observed that B7-H3-T-A-C-T was associated with the decreased release of sB7-H3 but not the membrane form.

Conclusions

B7-H3 may act as a potential biomarker related to the pathogenesis of T1D. The B7-H3-T-A-C-T polymorphism variant is associated with the low risk of T1D as well as less release of sB7-H3.

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Most cited references 22

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Tim-3 inhibits T helper type 1-mediated auto- and alloimmune responses and promotes immunological tolerance.

Alberto Sanchez-Fueyo, Jane Tian, Dominic Picarella … (2003)

Although T helper (T(H)) cell-mediated immunity is required to effectively eliminate pathogens, unrestrained T(H) activity also contributes to tissue injury in many inflammatory and autoimmune diseases. We report here that the T(H) type 1 (T(H)1)-specific Tim-3 (T cell immunoglobulin domain, mucin domain) protein functions to inhibit aggressive T(H)1-mediated auto- and alloimmune responses. Tim-3 pathway blockade accelerated diabetes in nonobese diabetic mice and prevented acquisition of transplantation tolerance induced by costimulation blockade. These effects were mediated, at least in part, by dampening of the antigen-specific immunosuppressive function of CD4(+)CD25(+) regulatory T cell populations. Our data indicate that the Tim-3 pathway provides an important mechanism to down-regulate T(H)1-dependent immune responses and to facilitate the development of immunological tolerance.

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The T1D Exchange clinic registry.

Dewayne Dubose, William Tamborlane, Robert Miller … (2012)

The T1D Exchange includes a clinic-based registry, a patient-centric web site called Glu, and a biobank. The aim of the study was to describe the T1D Exchange clinic registry and provide an overview of participant characteristics. Data obtained through participant completion of a questionnaire and chart extraction include diabetes history, management, and monitoring; general health; lifestyle; family history; socioeconomic factors; medications; acute and chronic diabetic complications; other medical conditions; and laboratory results. Data were collected from 67 endocrinology centers throughout the United States. We studied 25,833 adults and children with presumed autoimmune type 1 diabetes (T1D). Participants ranged in age from less than 1 to 93 yr, 50% were female, 82% were Caucasian, 50% used an insulin pump, 6% used continuous glucose monitoring, and 16% had a first-degree family member with T1D. Glycosylated hemoglobin at enrollment averaged 8.3% and was highest in 13 to 25 yr olds. The prevalence of renal disease was ≤4% until T1D was present for at least 10 yr, and retinopathy treatment was ≤2% until T1D was present for at least 20 yr. A severe hypoglycemic event (seizure or coma) in the prior 12 months was reported by 7% of participants and diabetic ketoacidosis in the prior 12 months by 8%. The T1D Exchange clinic registry provides a database of important information on individuals with T1D in the United States. The rich dataset of the registry provides an opportunity to address numerous issues of relevance to clinicians and patients, including assessments of associations between patient characteristics and diabetes management factors with outcomes.

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B7 family checkpoint regulators in immune regulation and disease.

R. Noelle, Sabrina Ceeraz, Elizabeth C Nowak (2013)

Fine-tuning the immune response and maintaining tolerance to self-antigens involves a complex network of co-stimulatory and co-inhibitory molecules. The recent FDA approval of ipilimumab, a monoclonal antibody blocking cytotoxic T lymphocyte antigen (CTLA)-4, demonstrates the impact of checkpoint regulators in disease. This is reinforced by ongoing clinical trials targeting not only CTLA-4, but also the programmed death (PD)-1 and B7-H4 pathways in various disease states. Recently, two new B7 family inhibitory ligands, V-domain Ig suppressor of T cell activation (VISTA) and B7-H6 were identified. Here, we review recent understanding of B7 family members and their concerted regulation of the immune response to either self or foreign pathogens. We also discuss clinical developments in targeting these pathways in different disease settings, and introduce VISTA as a putative therapeutic target. Copyright © 2013 Elsevier Ltd. All rights reserved.

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Author and article information

Contributors

Cuiping Liu: liucuiping1980@126.com

Chen Fang: afa9911@sina.com

Journal

Journal ID (nlm-ta): BMC Endocr Disord

Journal ID (iso-abbrev): BMC Endocr Disord

Title: BMC Endocrine Disorders

Publisher: BioMed Central (London )

ISSN (Electronic): 1472-6823

Publication date (Electronic): 12 August 2020

Publication date PMC-release: 12 August 2020

Publication date Collection: 2020

Volume: 20

Electronic Location Identifier: 123

Affiliations

[1 ]GRID grid.429222.d, ISNI 0000 0004 1798 0228, Jiangsu Institute of Clinical Immunology & Jiangsu Key Laboratory of Clinical Immunology, , First Affiliated Hospital of Soochow University, ; Suzhou, 215007 Jiangsu People’s Republic of China

[2 ]GRID grid.452666.5, ISNI 0000 0004 1762 8363, Department of Endocrinology, , Second Affiliated Hospital of Soochow University, ; Suzhou, 215004 Jiangsu People’s Republic of China

[3 ]GRID grid.488140.1, Institute of Medical Biotechnology, Suzhou Health College, ; Suzhou, 215009 Jiangsu People’s Republic of China

Article

Publisher ID: 592

DOI: 10.1186/s12902-020-00592-7

PMC ID: 7425597

PubMed ID: 32787907

SO-VID: 865c35b7-3126-48c9-be6a-2ce93deab37d

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 20 September 2019

Date accepted : 13 July 2020

Funding

Funded by: National Natural Science Foundation of China (CN)

Award ID: 81873876

Award Recipient : Cuiping Liu

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: 81801595

Award ID: 31700778

Award ID: 81600607

Award Recipient : Xin Chang Ziyi Huang Chen Fang

Custom metadata

ScienceOpen disciplines: Endocrinology & Diabetes

Keywords: type 1 diabetes,snp,mb7-h3,sb7-h3

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ScienceOpen disciplines: Endocrinology & Diabetes

Keywords: type 1 diabetes, snp, mb7-h3, sb7-h3

Evaluation of the role of B7-H3 haplotype in association with impaired B7-H3 expression and protection against type 1 diabetes in Chinese Han population

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Abstract

Background

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Conclusions

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Journal of the ASEAN Federation of Endocrine Societies

Most cited references 22

Tim-3 inhibits T helper type 1-mediated auto- and alloimmune responses and promotes immunological tolerance.

The T1D Exchange clinic registry.

B7 family checkpoint regulators in immune regulation and disease.

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