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Molecular Mechanisms and Targeted Regulation of Autoimmune Diseases

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 February 2026) | Viewed by 6408

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Dr. Davide Raineri

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Department of Health Sciences, Center for Translational Research on Autoimmune and Allergic Disease-CAAD, Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy
Interests: osteopontin; cancers; autoimmune diseases; inflammation; chronic diseases
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Special Issue Information

Dear Colleagues,

Cutting-edge molecular research in autoimmunity is a new scientific area that could transform our understanding and treatment of autoimmune diseases. At its core, this field delves into the intricate mechanisms underlying how the immune system, designed to protect the body, can mistakenly attack its own tissues. Researchers are leveraging sophisticated molecular techniques to pinpoint genetic predispositions, epigenetic modifications, and environmental triggers that contribute to autoimmune conditions.

Key areas of focus include identifying specific biomarkers that can predict disease onset or progression, unraveling the complex interplay of immune cells and signaling molecules, and developing targeted therapies that modulate immune responses with precision. Techniques such as genome-wide association studies (GWASs), single-cell RNA sequencing, advanced imaging technologies, and high-dimensional flow cytometry are driving breakthroughs in understanding disease pathogenesis at unprecedented levels of detail.

Moreover, cutting-edge research is paving the way for personalized medicine approaches, where treatments can be tailored to an individual’s genetic and molecular profile, potentially optimizing therapeutic outcomes and minimizing side effects. As these molecular insights continue to deepen, they offer hope for novel therapies that may one day provide effective management or even cures for autoimmune diseases, significantly improving millions of individuals’ quality of life worldwide.

This Special Issue welcomes submissions on the latest advancements in the molecular research of autoimmune diseases, particularly original research and review articles focusing on biomarker identification, immune cell and signaling molecule interactions, and the development of personalized therapeutic strategies. Through these high-quality contributions, we aim to foster scientific discoveries and applications in this promising field.

Dr. Davide Raineri
Guest Editor

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Keywords

autoimmunity
autoimmune diseases
multiple sclerosis
rheumatoid arthritis
lupus
type 1 diabetes
inflammatory bowel disease
biomarkers
immune cells
signaling molecules

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Published Papers (5 papers)

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Research

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9 pages, 5630 KB

Open AccessArticle

Cell-Targeted Inhibition of CaMK4 Suppresses Tertiary Lymphoid-like Structure Development in Lupus-Prone Mice

by Simin Jamaly, Mehrdad Rakaee, Kunihiro Ichinose, Kayaho Maeda, Kotaro Otomo, Tomohiro Koga, Maria G. Tsokos and George C. Tsokos

Int. J. Mol. Sci. 2026, 27(7), 3190; https://doi.org/10.3390/ijms27073190 - 31 Mar 2026

Viewed by 451

Abstract

Current treatment of lupus nephritis (LN) relies on broad immunosuppression and often fails to eradicate intrarenal immune niches that sustain inflammation. Tertiary lymphoid structures (TLS)—organized aggregates of immune cells forming in chronically inflamed non-lymphoid tissues—are increasingly recognized as drivers of local immune activation and tissue injury in LN. We previously showed that genetic CaMK4 deficiency suppresses autoimmunity and nephritis in lupus-prone mice. Here, we tested whether CaMK4 regulates renal TLS-like organization. Using kidneys from MRL/lpr mice that were CaMK4-deficient or treated with KN93-loaded nanoparticles targeted to CD4⁺ T cells or podocytes (anti-podocin), we compared findings with vehicle-treated controls. TLS-associated inflammation and maturation were quantified by mean fluorescence intensity of CD3, CD20, Ki67, and α-SMA. Across genetic and targeted-treatment arms, CaMK4 inhibition reduced all assessed markers, with uniform suppression of CD20 signal, highlighting a key role for B cells in TLS maintenance. Notably, podocyte-targeted KN93 most strongly suppressed TLS-like formation, implicating podocyte-driven pathways in interstitial inflammation and lymphoid neogenesis through previously underappreciated mechanisms. These data identify CaMK4 as a regulator of TLS-like architecture in LN and support the translational potential of cell-targeted CaMK4 inhibition to disrupt local immune recruitment while limiting systemic toxicity. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Targeted Regulation of Autoimmune Diseases)

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14 pages, 915 KB

Open AccessArticle

Serum Cocaine- and Amphetamine-Regulated Transcript (CART) Levels in Graves’ Disease: Associations with Metabolic Status, Autoimmunity, and Thyroid Ultrasound Heterogeneity

by Betül Çiğdem Yortanlı, Ümmügülsüm Can, İslam Köse, Semiha Durmaz, Mehmet Yortanlı and Oğuzhan Aksu

Int. J. Mol. Sci. 2026, 27(5), 2428; https://doi.org/10.3390/ijms27052428 - 6 Mar 2026

Viewed by 449

Abstract

Graves’ disease (GD) is an autoimmune disorder characterized by hyperthyroidism and a hypermetabolic state involving complex endocrine, metabolic, and immune interactions. Cocaine- and amphetamine-regulated transcript (CART) is a neuropeptide involved in energy balance, neuroendocrine signaling, and neuroimmune modulation; however, its circulating levels and clinical relevance in GD remain unclear. In this single-center prospective study, serum CART levels were evaluated in 44 patients with GD and 44 age- and sex-matched healthy controls. Associations with thyroid function, autoimmune markers, metabolic parameters, and thyroid ultrasound heterogeneity were analyzed. Serum CART concentrations were measured using an enzyme-linked immunosorbent assay, and clinical, biochemical, and ultrasonographic data were recorded. Serum CART levels did not differ significantly between GD patients and healthy controls. However, within the GD group, CART levels varied significantly according to thyroid ultrasound heterogeneity, with lower levels observed in patients with severe parenchymal heterogeneity. Serum CART levels showed positive correlations with body mass index and insulin resistance indices, while inverse correlations were observed with thyrotropin receptor antibody and anti-thyroid peroxidase antibody levels. No significant associations were identified between serum CART levels and circulating thyroid hormone concentrations. These findings suggest that serum CART may reflect metabolic and autoimmune heterogeneity rather than hypothalamic–pituitary–thyroid axis activity in GD, supporting its role as a context-sensitive, hypothesis-generating biomarker. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Targeted Regulation of Autoimmune Diseases)

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15 pages, 2417 KB

Open AccessArticle

The Association of Anti-Sm with Osteopontin Related to Cognitive Impairment in a Pristane-Induced Lupus BALB/c Mice Model

by Daniel González-Inostroz, Flavio Sandoval-García, Fernanda-Isadora Corona-Meraz, Mónica Vázquez Del Mercado, Jorge Guzmán-Muñiz, Milton Omar Guzmán-Ornelas, Rolando Castañeda-Arellano, Jacinto Bañuelos-Pineda, Miguel Peña-Nava and Beatriz-Teresita Martín-Márquez

Int. J. Mol. Sci. 2024, 25(23), 13080; https://doi.org/10.3390/ijms252313080 - 5 Dec 2024

Cited by 3 | Viewed by 2088

Abstract

The BALB/c model of pristane-induced lupus (PIL) exhibits cognitive impairment features resembling neuropsychiatric lupus (NPLSE). Osteopontin (OPN) is associated with disease activity in SLE; however, its involvement in NPLSE is not yet entirely determined. Our study aims to elucidate the contribution of full-length OPN (OPN-FL) plasma expression, OPN N-half, and Spp1 to cognitive impairment in the PIL mice model. A total of 76 female BALB/c mice were divided into pristane (P), pristane plus lipopolysaccharide (P plus LPS) and control (C) groups. In behavioral tests, the P group showed cognitive and visuospatial memory impairment. Elevated plasma OPN FL levels were found in P compared to C groups (177.7 ± 90.1 vs. 105.9 ± 56.8 ng/mL, p = 0.009) and OPN N-half was different between P and C groups (673.5 ± 144.6 vs. 624.5 ± 377.7 ng/mL, p = 0.028) and P plus LPS and C groups (624.5 ± 377.7 vs. 381.4 ± 205.0 ng/mL, p = 0.001). Anti-Sm correlated with OPN-FL (r = 0.269, p = 0.0150). The relative expression of Spp1 in the brain was 2.5 and 2.7-fold higher in P and P plus LPS groups, respectively. The evidence suggests that OPN is related to cognitive impairment in PIL mice and might play a relevant role in the detrimental neurological conditions of NPSLE. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Targeted Regulation of Autoimmune Diseases)

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Review

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33 pages, 1255 KB

Open AccessReview

Cellular Immunotherapies for Multiple Sclerosis: Mechanistic Insights and Clinical Advances

by Vasily Kurilin, Marina Fisher, Irina Obleukhova and Sergey Sennikov

Int. J. Mol. Sci. 2026, 27(2), 585; https://doi.org/10.3390/ijms27020585 - 6 Jan 2026

Viewed by 1205

Abstract

Multiple sclerosis (MS) is a chronic, heterogeneous, multifactorial, immune-mediated neurodegenerative disease of the central nervous system that affects the working-age population. Its development is influenced by both genetic and environmental factors. A pathological hallmark of MS is the formation of demyelinating lesions in the brain and spinal cord, which are associated with neuronal damage caused by autoaggressive immune factors (T cells, B cells, and myeloid cells). Focal lesions are believed to be caused by the infiltration of immune cells into the central nervous system (CNS) parenchyma with concomitant tissue damage. Multiple sclerosis represents a significant social problem due to the high cost of available treatments, as well as the deterioration of employment prospects and job retention for both patients and their caregivers. Advances in MS diagnostic methods have enabled disease detection at early stages and correction of immune response impairments. Concurrently, treatments for MS patients are actively being studied, with the ongoing development of novel methods for targeted and cellular immunotherapy. This review primarily discusses approaches to cellular immunotherapy and methods of influencing the cellular arm of immunopathogenesis in multiple sclerosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Targeted Regulation of Autoimmune Diseases)

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Other

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10 pages, 660 KB

Open AccessBrief Report

Detection and Clinical Associations of Autoantibodies to Heterogeneous Nuclear Ribonucleoprotein (hnRNP) A2/B1 in Patients with Systemic Sclerosis

by Antonio Tonutti, Natasa Isailovic, Lukas Frischknecht, Francesca Motta, Minoru Satoh, Carlo Selmi, Maria De Santis and Angela Ceribelli

Int. J. Mol. Sci. 2025, 26(18), 8892; https://doi.org/10.3390/ijms26188892 - 12 Sep 2025

Cited by 1 | Viewed by 1057

Abstract

Autoantibodies targeting heterogeneous nuclear ribonucleoproteins (hnRNPs) have been seldom described in autoimmune diseases but remain poorly characterized in systemic sclerosis (SSc). This study aims to investigate the prevalence and clinical significance of anti-hnRNP autoantibodies in SSc. Serum samples from 25 well-characterized SSc patients were analyzed using protein immunoprecipitation (IP) to detect autoantibodies against hnRNP components A1, A2/B1, C1/C2, H, L, and U. Clinical data including organ involvement and autoantibody profiles were also collected over a 10-year follow-up period. Anti-hnRNP A2/B1 autoantibodies were identified in 40% of SSc patients and significantly associated with gastrointestinal involvement (80% vs. 27%; p = 0.015; OR 17, 95% CI 2.2–381). Additional components such as anti-hnRNP L antibodies exhibited variable protein-IP band patterns, with a trend toward an association between a “double” band pattern and cancer history (p = 0.066). Anti-hnRNP U antibodies were detected in a single patient presenting with severe digital ulcers. No patient tested positive for antibodies against other components, including A1, C1/C2, and H. In this preliminary hypothesis-generating study, anti-hnRNP autoantibodies were frequent in SSc patients with distinct prevalence and clinical associations depending on the target component. Anti-hnRNP A2/B1 correlate with gastrointestinal involvement but, contrary to previous reports, show no association with arthritis. Further exploration on anti-hnRNP L and the rarer anti-hnRNP U autoantibodies is warranted. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Targeted Regulation of Autoimmune Diseases)

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