Pharmacological Modulation of Inflammation in Autoimmune Diseases and Cancer

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 27 January 2026 | Viewed by 863

Special Issue Editors


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Guest Editor
Department of Health Sciences, Università del Piemonte Orientale UPO, 28100 Novara, Italy
Interests: microenvironment; tumor targeting; pharmacokinetics; toxicology; telomerase; nanoparticles for drug delivery; chemotherapy; pharmacodynamics; inflammation; neurosciences in cancer
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy
Interests: inflammation; innate immunity; immunity; cancer biology; cellular immunology; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation is a complex biological response crucial for host defense, tissue repair, and the cancer microenvironment. However, its dysregulation contributes to the pathogenesis of autoimmune diseases and cancer. In autoimmune disorders, the aberrant activation of immune pathways leads to chronic inflammation, resulting in tissue damage and organ dysfunction. Conversely, in cancer, the inflammatory microenvironment can both promote tumor initiation and support progression by fostering angiogenesis, immune evasion, and metastasis.

Recent pharmacological advances have focused on targeting key inflammatory mediators and signaling pathways shared across autoimmune diseases and cancer. Small molecules, monoclonal antibodies, and biologics targeting cytokines such as TNF-α, IL-6, and IL-17, as well as intracellular signaling cascades like JAK/STAT and NF-κB, have demonstrated significant clinical efficacy in diseases such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. Simultaneously, these inflammatory axes are increasingly recognized as pivotal in the tumor microenvironment, offering novel targets for cancer therapy.

Moreover, immune checkpoint inhibitors, while revolutionizing cancer treatment, often trigger immune-related adverse events resembling autoimmune conditions, highlighting the intertwined nature of immune modulation in these pathologies. Thus, a deeper understanding of inflammation’s dualistic role is critical for developing therapeutics that can finely tune immune responses without tipping the balance toward pathological autoimmunity or immune escape in cancer.

This Special Issue invites original research manuscripts and reviews focusing on innovative pharmacological strategies to modulate inflammation in autoimmune diseases and cancer. We welcome studies on novel drug candidates, repurposing existing agents, mechanisms of action, biomarker discovery, and translational approaches that bridge basic immunology with clinical application. Contributions addressing the challenges of balancing clinical efficacy with safety in immunomodulatory therapy and basic biology research in this field are particularly encouraged.

Dr. Donato Colangelo
Dr. Stelvio Tonello
Guest Editors

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Keywords

  • microenvironment
  • TRAP
  • NET
  • tumor niche
  • exosomes
  • neuromodulation of tumor growth
  • autoimmune diseases
  • pharmacology
  • biomarkers

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Published Papers (1 paper)

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33 pages, 4098 KB  
Systematic Review
Pharmacological Inhibition of the PI3K/AKT/mTOR Pathway in Rheumatoid Arthritis Synoviocytes: A Systematic Review and Meta-Analysis (Preclinical)
by Tatiana Bobkova, Artem Bobkov and Yang Li
Pharmaceuticals 2025, 18(8), 1152; https://doi.org/10.3390/ph18081152 - 2 Aug 2025
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Abstract
Background/Objectives: Constitutive activation of the PI3K/AKT/mTOR signaling cascade underlies the aggressive phenotype of fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA); however, a quantitative synthesis of in vitro data on pathway inhibition remains lacking. This systematic review and meta-analysis aimed to (i) aggregate [...] Read more.
Background/Objectives: Constitutive activation of the PI3K/AKT/mTOR signaling cascade underlies the aggressive phenotype of fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA); however, a quantitative synthesis of in vitro data on pathway inhibition remains lacking. This systematic review and meta-analysis aimed to (i) aggregate standardized effects of pathway inhibitors on proliferation, apoptosis, migration/invasion, IL-6/IL-8 secretion, p-AKT, and LC3; (ii) assess heterogeneity and identify key moderators of variability, including stimulus type, cell source, and inhibitor class. Methods: PubMed, Europe PMC, and the Cochrane Library were searched up to 18 May 2025 (PROSPERO CRD420251058185). Twenty of 2684 screened records met eligibility. Two reviewers independently extracted data and assessed study quality with SciRAP. Standardized mean differences (Hedges g) were pooled using a Sidik–Jonkman random-effects model with Hartung–Knapp confidence intervals. Heterogeneity (τ2, I2), 95% prediction intervals, and meta-regression by cell type were calculated; robustness was tested with REML-HK, leave-one-out, and Baujat diagnostics. Results: PI3K/AKT/mTOR inhibition markedly reduced proliferation (to –5.1 SD), IL-6 (–11.1 SD), and IL-8 (–6.5 SD) while increasing apoptosis (+2.7 SD). Fourteen of seventeen outcome clusters showed large effects (|g| ≥ 0.8), with low–moderate heterogeneity (I2 ≤ 35% in 11 clusters). Prediction intervals crossed zero only in small k-groups; sensitivity analyses shifted pooled estimates by ≤0.05 SD. p-AKT and p-mTOR consistently reflected functional changes and emerged as reliable pharmacodynamic markers. Conclusions: Targeted blockade of PI3K/AKT/mTOR robustly suppresses the proliferative and inflammatory phenotype of RA-FLSs, reaffirming this axis as a therapeutic target. The stability of estimates across multiple analytic scenarios enhances confidence in these findings and highlights p-AKT and p-mTOR as translational response markers. The present synthesis provides a quantitative basis for personalized dual-PI3K/mTOR strategies and supports the adoption of standardized long-term preclinical protocols. Full article
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