This review includes an overview of autoimmune T1D, immune cells involved in T1D pathophysiology, and immunotherapy-based strategies to treat and prevent autoimmune T1D. Innovative approaches must be developed to counteract pancreatic β-cell destruction and salvage endogenic insulin production, thereby regulating blood glucose levels. However, this strategy is not feasible due to several obstacles, including a scarcity of donors, islet cells, and poor vascular engraftment of islets post-transplantation, as well as the need for prolonged immune suppression. Transplantation of primary pancreatic islets or the entire pancreas is a viable remedy for managing patients with autoimmune T1D. Continuous exogenous insulin replacement therapy is the current standard of care for T1D. Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing pancreatic β-cells by their own immune system, resulting in lifelong insulin deficiency. These areas will be explored using examples from several autoimmune diseases but will focus mainly on type 1 diabetes. The effects of these various signals on disease progression and the relative effects of DC subset composition and maturation level of DCs will be examined. Specific topics to be addressed include impact of susceptibility loci on DC subsets, alterations in DC subset development, the role of infection- and host-derived innate inflammatory signals, and the role of the intestinal microbiota on DC phenotype. In this review, we will discuss the role of these subsets in autoimmune pathogenesis and regulation, as well as the genetic and environmental signals that influence their function. Although the specific DC phenotype can diverge depending on the tissue location and context, there are four main subsets identified in both mouse and human: conventional cDC1 and cDC2, plasmacytoid DCs, and monocyte-derived DCs.
The balance between these two outcomes depends on several factors, including genetic susceptibility, environmental signals that stimulate varied innate responses, and which DC subset is presenting antigen. DCs control both steady-state T cell tolerance and activation of pathogenic responses. Dendritic cells (DCs) are key antigen-presenting cells that have an important role in autoimmune pathogenesis.
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