Abstract
ObjectivesFollicular helper T (Tfh) cells exert an important role in autoimmune diseases. Whether it might be involved in type 1 diabetes (T1D) is unknown. Our aim was to investigate the role of Tfh cells in patients with T1D and the effect of anti-CD20 monoclonal antibody (rituximab) on Tfh cells from T1D patients.Patients and MethodsFifty-four patients with T1D and 37 healthy controls were enrolled in the current study. 20 of those patients were treated with rituximab. The frequencies of circulating CD4+CXCR5+ICOS+T cells were analyzed by flow cytometry. The serum autoantibodies were detected by radioligand assay. The levels of IL-21, IL-6 and BCL-6 were assessed using ELISA and/or real-time PCR.ResultsIncreased frequencies of circulating Tfh cells together with enhanced expression of IL-21 were detected in patients. The correlation between the frequencies of circulating Tfh cells and the serum autoantibodies or C-peptide level was comfirmed. After rituximab therapy, follow-up analysis demonstrated that the frequencies of circulating Tfh cell and serum IA2A were decreased. The levels of IL-21, IL-6 and Bcl-6 mRNA were decreased after treatment. Furthermore, beta cell function in 10 of 20 patients was improved.ConclusionsThese data indicate Tfh cells may participate in the T1D-relatede immune responses and B cells might play a role in the development of Tfh responses in the disease progression.
Highlights
Type 1 diabetes (T1D) is a disease resulting from the specific destruction of beta cells within pancreatic islets by autoreactive CD4+ and CD8+ T cells
Follow-up analysis demonstrated that the frequencies of circulating T follicular helper (Tfh) cell and serum IA2A were decreased
Beta cell function in 10 of 20 patients was improved. These data indicate Tfh cells may participate in the T1D-relatede immune responses and B cells might play a role in the development of Tfh responses in the disease progression
Summary
Type 1 diabetes (T1D) is a disease resulting from the specific destruction of beta cells within pancreatic islets by autoreactive CD4+ and CD8+ T cells. T cells are dominant determinants of beta-cell destruction in NOD mice and humans, B cells and humoral immunity may play a role in T1D development or disease progression [1]. B cells infiltrate the pancreatic islets of NOD mice during the autoimmune response that precedes the onset of type 1 diabetes [2]. They may contribute to diabetes in NOD mice by supporting development of tertiary lymphoid structures in the vicinity of pancreatic islets where pathogenic T cells might be activated [3]. The importance of B cells in Type 1 diabetes has been resurrected based on the clinical efficacy of B cell depletion with anti-CD20 (rituximab) in T1D patients [6]
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