Increased plasmablasts enhance T cell-mediated beta cell destruction and promote the development of type 1 diabetes

• Published in: Molecular medicine (Cambridge, Mass.) Vol. 28; no. 1; pp. 18 - 16
• Main Authors: Ling, Qing, Shen, Lei, Zhang, Wei, Qu, DuoDuo, Wang, Hongdong, Wang, Bin, Liu, Yong, Lu, Jing, Zhu, Dalong, Bi, Yan
• Format: Journal Article
• Language: English
• Published: England BioMed Central 05.02.2022; BMC
• Subjects: Animals; Antibodies; Antigens; Autoimmunity; B cell subset; Biomarkers; Case-Control Studies; Cells; Diabetes; Diabetes Mellitus, Type 1 - diagnosis; Diabetes Mellitus, Type 1 - etiology; Diabetes Mellitus, Type 1 - metabolism; Disease; Disease Models, Animal; Disease Susceptibility - immunology; Female; Flow cytometry; Humans; Immune response; Immunohistochemistry; Immunophenotyping; Immunotherapy; Insulin-Secreting Cells - immunology; Insulin-Secreting Cells - metabolism; Insulin-Secreting Cells - pathology; Ketosis; Lymphatic system; Lymphocyte Activation; Lymphocytes; Male; Mice; Mice, SCID; Pathogenesis; Peptides; Plasmablast; T cell; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; Type 1 diabetes; United States > US; Autoimmunity; B cell subset; Plasmablast; Type 1 diabetes; T cell

Although type 1 diabetes (T1D) is typically described as a T cell-mediated autoimmune disease, increasing evidence for a role of B cells has emerged. However, the pivotal disease-relevant B cell subset and its contribution to islet autoimmunity remain elusive. The frequencies and phenotypic characte...