T helper 17 cells and interleukin-17 immunity in type 1 diabetes: From pathophysiology to targeted immunotherapies

Figure 2 Natural history of type 1 diabetes and role of T helper 17 cells/interleukin-17 immunity in the pathophysiology of type 1 diabetes. Type 1 diabetes (T1D) stages are characterized by a progressive decline in beta-cell mass and function due to underlying autoimmune processes. A: Depicts the progressive decline in functional beta-cell mass throughout the sequential stages of T1D (stages of islet autoimmunity, dysglycemia and symptomatic disease); B: Illustrates the immune dysregulation observed in T1D, emphasizing the imbalance between pro-inflammatory T helper 17 (Th17) cells and regulatory T cells (Tregs). Th17 cells (involved in interleukin-17 production) promote beta-cell destruction, while Tregs (which physiologically maintain immune tolerance) are poorly represented and/or functionally impaired. This imbalance contributes to the immune-mediated destruction of insulin-producing beta cells and may be targeted by immunotherapies employed for the treatment of T1D. CD: Cluster of differentiation; T1D: Type 1 diabetes; IL-17: Interleukin-17; Th-17: T helper 17; FOXP3: Forkhead box P3; RORγt: Retinoic acid-related orphan receptor gamma t; Tregs: Regulatory T cells. Figure 2 was partly created with images adapted from Servier Medical Art licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0) (https://smart.servier.com/).