ArticlePloS one2014
Altered B cell homeostasis and toll-like receptor 9-driven response in type 1 diabetes carriers of the C1858T PTPN22 allelic variant: implications in the disease pathogenesis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Optimization of Lipoplexes Functionalized with a Sialic Acid Mimetic (F9-PEG) to Target the C1858TPharmaceutics · 2025Article
- Effect of the autoimmune-associated genetic variantFrontiers in immunology · 2025Article
- Improvement of Lipoplexes With a Sialic Acid Mimetic to Target the C1858TFrontiers in immunology · 2022Article
- Preparation and In Vitro Evaluation of RITUXfab-Decorated Lipoplexes to Improve Delivery of siRNA Targeting C1858T PTPN22 Variant in B Lymphocytes.International journal of molecular sciences · 2021Article
- Overexpression of theJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- De-coding genetic risk variants in type 1 diabetes.Immunology and cell biology · 2021Review
- p53 Activation Effect in the Balance of T Regulatory and Effector Cell Subsets in Patients With Thyroid Cancer and Autoimmunity.Frontiers in immunology · 2021Article
- Influence ofFrontiers in immunology · 2021Review
- Article
- Identification and functional characterization of CD8+ T regulatory cells in type 1 diabetes patients.PloS one · 2019Article
- Modulation of the immune system by the gut microbiota in the development of type 1 diabetes.Human vaccines & immunotherapeutics · 2018Article
- On the pathogenesis of insulin-dependent diabetes mellitus: the role of microbiota.Immunologic research · 2017Review
- Article
- Use of short interfering RNA delivered by cationic liposomes to enable efficient down-regulation of PTPN22 gene in human T lymphocytes.PloS one · 2017Article
- Antibody responses to de novo identified citrullinated fibrinogen peptides in rheumatoid arthritis and visualization of the corresponding B cells.Arthritis research & therapy · 2016Article
- Autoimmune Variant PTPN22 C1858T Is Associated With Impaired Responses to Influenza Vaccination.The Journal of infectious diseases · 2016Article
- The role of the innate immune system in destruction of pancreatic beta cells in NOD mice and humans with type I diabetes.Journal of autoimmunity · 2016Review
- Expression of PD-1 Molecule on Regulatory T Lymphocytes in Patients with Insulin-Dependent Diabetes Mellitus.International journal of molecular sciences · 2015Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes is an autoimmune disease caused by the destruction of pancreatic beta cells by autoreactive T cells. Among the genetic variants associated with type 1 diabetes, the C1858T (Lyp) polymorphism of the protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene alters the function of T cells but also of B cells in innate and adaptive immunity. The Lyp variant was shown to diminish interferon production and responses upon Toll-like receptor stimulation in macrophages and dendritic cells, possibly leading to uncontrolled infections as triggers of the diabetogenic process. The aim of this study was to unravel the yet uncharacterized effects that the variant could exert on the immune and autoimmune responses, particularly regarding the B cell phenotype, in the peripheral blood lymphocytes of diabetic patients and healthy controls in basal conditions and after unmethylated bacterial DNA CpG stimulation. The presence of the Lyp variant resulted in a significant increase in the percentage of transitional B cells in C/T carriers patients and controls compared to C/C patients and controls, in C/T carrier patients compared to C/C controls and in C/T carrier patients compared to C/C patients. A significant reduction in the memory B cells was also observed in the presence of the risk variant. After four days of CpG stimulation, there was a significant increase in the abundance of IgM+ memory B cells in C/T carrier diabetics than in C/C subjects and in the groups of C/T carrier individuals than in C/C individuals. IgM- memory B cells tended to differentiate more precociously into plasma cells than IgM+ memory B cells in heterozygous C/T subjects compared to the C/C subjects. The increased Toll-like receptor response that led to expanded T cell-independent IgM+ memory B cells should be further investigated to determine the putative contribution of innate immune responses in the disease pathogenesis.
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