Perspective - (2025) Volume 11, Issue 6
Received: 01-Dec-2025, Manuscript No. icoa-25-178185;
Editor assigned: 03-Dec-2025, Pre QC No. P-178185;
Reviewed: 17-Dec-2025, QC No. Q-178185;
Revised: 22-Dec-2025, Manuscript No. R-178185;
Published:
29-Dec-2025
, DOI: 10.37421/2469-9756.2025.11.334
Citation: Romano, Francesca. ”Immune Dysregulation Driving Autoimmune Diseases: Mechanisms and Therapies.” Immunochem Immunopathol 11 (2025):334.
Copyright: © 2025 Romano F. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
The intricate mechanisms driving immunopathogenesis in autoimmune diseases are a subject of intense research, with a significant focus on the dysregulation of T cell subsets and their aberrant interactions with antigen-presenting cells. This area of study seeks to unravel how molecular mimicry and environmental triggers can initiate autoimmune responses, leading to chronic inflammation and tissue damage. The complex interplay of specific cytokines and signaling pathways is crucial in perpetuating the disease state, and identifying potential therapeutic targets aimed at restoring immune tolerance is a primary goal in this field [1].
Further insight into the immunopathogenesis of autoimmune conditions comes from examining the contribution of B cell hyperactivity and autoantibody production. The signaling cascades involved in B cell activation and differentiation into antibody-secreting plasma cells are critical, with particular emphasis on the role of B cell-activating factor (BAFF) and its receptor. These findings underscore the importance of targeting B cell pathways for therapeutic intervention in diseases like systemic lupus erythematosus [2].
Innate immune cells also play a pivotal role in chronic inflammation, a hallmark of many autoimmune diseases. Macrophages and neutrophils, for instance, are activated and contribute to tissue destruction through the release of pro-inflammatory mediators and matrix metalloproteinases. Specific inflammasome complexes have been identified as key drivers of these inflammatory cascades, suggesting their potential as therapeutic targets in conditions such as rheumatoid arthritis [3].
The immunopathogenesis of inflammatory bowel disease (IBD) is characterized by a complex interplay between the gut microbiota, immune cells, and the intestinal epithelium. A breakdown in intestinal barrier function and aberrant activation of T helper 17 (Th17) cells are central to the disease process. Research in this area discusses the potential of targeting gut microbial dysbiosis and Th17-related cytokines for IBD treatment [4].
Regulatory T cells (Tregs) are essential for maintaining immune tolerance, and their dysfunction is implicated in the immunopathogenesis of various autoimmune conditions. Understanding the mechanisms by which Tregs suppress immune responses and how their defects lead to autoimmune diseases is crucial. Exploring strategies to enhance Treg function offers a promising therapeutic approach for these conditions [5].
The immunopathogenesis of type 1 diabetes is largely driven by the autoimmune destruction of pancreatic beta cells, primarily mediated by T cells. The process involves antigen presentation and T cell receptor signaling, which initiate and perpetuate the autoimmune attack. The involvement of specific autoantigens and their presentation by antigen-presenting cells in pancreatic lymph nodes is a key aspect of this disease [6].
The complement system's activation contributes significantly to the immunopathogenesis of diverse autoimmune diseases, including lupus nephritis and Guillain-Barré syndrome. Complement proteins can directly damage tissues and amplify inflammatory responses, thereby exacerbating disease severity. Consequently, complement inhibition is being explored as a promising therapeutic strategy [7].
Cytokine dysregulation is a critical factor in the immunopathogenesis of conditions like psoriasis. Specific pro-inflammatory cytokines, such as TNF-alpha, IL-17, and IL-23, are known to promote keratinocyte hyperproliferation and chronic skin inflammation. Current and emerging biologic therapies are increasingly targeting these cytokine pathways for treatment [8].
The immunopathogenesis of multiple sclerosis (MS) involves self-reactive T cells targeting myelin antigens in the central nervous system. The breakdown of the blood-brain barrier allows immune cell infiltration, leading to demyelination and neuroinflammation. The contribution of glial cells and the impact of different T cell subsets on disease progression are areas of active investigation [9].
Sjögren's syndrome exemplifies immunopathogenesis driven by an autoimmune attack against exocrine glands. The infiltration of lymphocytes and plasma cells into salivary and lacrimal glands results in impaired function. The roles of B cells, autoantibodies, and T cell cytokines are central to driving glandular inflammation and destruction in this condition [10].
The immunopathogenesis of autoimmune diseases is intricately linked to the dysregulation of T cell subsets and their aberrant interactions with antigen-presenting cells, initiating autoimmune responses through molecular mimicry and environmental triggers, leading to chronic inflammation and tissue damage. The identification of specific cytokines and signaling pathways that perpetuate disease states is paramount for developing therapeutic targets aimed at restoring immune tolerance [1].
In the context of systemic lupus erythematosus, B cell hyperactivity and subsequent autoantibody production play a significant role in immunopathogenesis. Detailed studies of the signaling cascades governing B cell activation and differentiation into antibody-secreting plasma cells, with a specific focus on the B cell-activating factor (BAFF) pathway, highlight potential avenues for therapeutic intervention by targeting these B cell-centric mechanisms [2].
In rheumatoid arthritis, innate immune cells such as macrophages and neutrophils are crucial contributors to chronic inflammation and joint destruction. Their activation leads to the release of pro-inflammatory mediators and matrix metalloproteinases, with inflammasome complexes identified as key drivers of the inflammatory cascade, presenting therapeutic opportunities through their targeted inhibition [3].
Inflammatory bowel disease (IBD) pathogenesis involves a complex interplay between the gut microbiota, immune cells, and the intestinal epithelium. The breakdown of intestinal barrier function and the aberrant activation of T helper 17 (Th17) cells are central features. Strategies targeting gut microbial dysbiosis and Th17-related cytokines are being explored for effective IBD treatment [4].
Regulatory T cells (Tregs) are fundamental to maintaining immune tolerance, and their functional defects are implicated in the immunopathogenesis of autoimmune conditions. Research into the mechanisms of Treg suppression and the consequences of their dysregulation is crucial for developing therapies that enhance Treg function to combat autoimmune diseases [5].
The immunopathogenesis of type 1 diabetes is characterized by T cell-mediated autoimmune destruction of pancreatic beta cells. The process is initiated and perpetuated by antigen presentation and T cell receptor signaling, with specific autoantigens presented by antigen-presenting cells in pancreatic lymph nodes playing a critical role in this autoimmune attack [6].
The complement system's activation contributes to the immunopathogenesis of various autoimmune diseases, including lupus nephritis and Guillain-Barré syndrome, by directly damaging tissues and amplifying inflammatory responses. This exacerbation of disease severity suggests that strategies involving complement inhibition hold promise as therapeutic interventions [7].
Cytokine networks are central to the immunopathogenesis of psoriasis, with pro-inflammatory cytokines like TNF-alpha, IL-17, and IL-23 driving keratinocyte hyperproliferation and chronic skin inflammation. The development of biologic therapies that target these specific cytokine pathways represents a significant advancement in managing psoriasis [8].
Multiple sclerosis (MS) immunopathogenesis involves self-reactive T cells that target myelin antigens in the central nervous system, leading to demyelination and neuroinflammation through the breakdown of the blood-brain barrier and immune cell infiltration. The interplay of glial cells and various T cell subsets significantly influences disease progression in MS [9].
Sjögren's syndrome immunopathogenesis is characterized by an autoimmune assault on exocrine glands, marked by lymphocyte and plasma cell infiltration leading to functional impairment. The combined actions of B cells, autoantibodies, and T cell cytokines are instrumental in driving this glandular inflammation and destruction [10].
This collection of research articles explores the complex immunopathogenesis of various autoimmune diseases. Key themes include the dysregulation of T and B cell subsets, the role of innate immune cells like macrophages and neutrophils, and the impact of cytokines and the complement system in driving chronic inflammation and tissue damage. Specific diseases examined include autoimmune diseases broadly, systemic lupus erythematosus, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, psoriasis, multiple sclerosis, and Sjögren's syndrome. The research highlights the importance of molecular mimicry, environmental triggers, and gut microbiota in initiating disease. Several studies point towards therapeutic strategies targeting specific immune cells, signaling pathways, cytokines, and the complement system to restore immune tolerance and manage these debilitating conditions. Regulatory T cells are identified as crucial for maintaining immune homeostasis and their dysfunction contributes to disease development.
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