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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 May 2026) | Viewed by 3529

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Prof. Dr. Pio Conti

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Postgraduate Medical School, University of Chieti, Chieti, Italy
Interests: inflammation; innate immunity; cell culture; immunology of infectious diseases; psoriasis
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Dear Colleagues,

Cytokines are mediators of the immune system and inflammatory diseases and play an important role in clinical pathogenesis. Cytokines are proteins produced primarily by immune cells such as T lymphocytes, macrophages, dendritic cells, neutrophils, basophils, and mast cells. In addition, fibroblasts, endothelial cells, epithelial cells, and other cells can also produce cytokines. Cytokines function as intercellular messengers that regulate the inflammatory and immune response. They can be classified based on their function: pro-inflammatory, such as TNF, IL-1, IL-6, IL-8, IFN-γ, and others; and anti-inflammatory, which limit the immune response, such as IL-10, TGF-β, IL-37, IL-1RA, IL-38, etc. Cytokine receptors are specific membrane proteins that activate intracellular signaling pathways. Type I and II receptors activate JAK-STAT signaling, while IL-1/TLR-like receptors activate the MyD88 pathway with the formation of NF-κB/MAPK. Cytokines are involved in many inflammatory diseases, including rheumatoid arthritis, where they activate the synovial joints and cause cartilage and bone destruction. In Crohn's disease/ulcerative colitis, they cause chronic intestinal inflammation and Th1/Th17 dysregulation, and in psoriasis, they mediate keratinocyte proliferation and dermal inflammation.

Prof. Dr. Pio Conti
Guest Editor

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Keywords

inflammation
cytokines
interleukin-6
immune diseases
immune signaling
autoimmunity
brain inflammation

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Published Papers (4 papers)

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Review

15 pages, 6918 KB

Open AccessReview

Proteomic Changes in Patients with LADA-Type Diabetes: Prospects for Diagnostic Biomarkers

by Adam Osowski, Tomasz Antonowski and Joanna Wojtkiewicz

Int. J. Mol. Sci. 2026, 27(12), 5205; https://doi.org/10.3390/ijms27125205 - 9 Jun 2026

Viewed by 83

Abstract

Latent autoimmune diabetes in adults (LADA) is a form of diabetes with clinical and biological features overlapping those of type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM), which may complicate early diagnosis and disease classification. Interest in proteomic and related biomarker profiles in LADA has increased in recent years because these markers may improve understanding of its pathophysiology and support more accurate differentiation from other forms of diabetes. This narrative review provides a structured overview of currently available evidence on selected inflammatory, immunological, and metabolic biomarkers associated with LADA. The reviewed literature includes data on adiponectin, IFN-γ, CCL2/MCP-1, IL-6, GPLD1, and other markers potentially linked to immune dysregulation, low-grade inflammation, and progressive β-cell dysfunction. Several studies suggest that LADA may present an intermediate biomarker profile, with some features overlapping with T1DM and others with T2DM. At the same time, the available evidence remains heterogeneous and is limited mainly by small sample sizes, cross-sectional designs, and incomplete clinical validation. Therefore, although several biomarkers appear promising for further investigation, their current role should be regarded as exploratory rather than established for routine clinical use. Further longitudinal and well-characterized studies are needed to determine whether selected biomarker patterns may eventually contribute to improved identification and stratification of LADA. Full article

(This article belongs to the Special Issue Cytokines and Inflammatory Diseases)

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22 pages, 8047 KB

Open AccessReview

Pro-Inflammatory Cytokines as Core Mediators of Colonic Epithelial Barrier Dysfunction: Roles of TNF-α, IFN-γ, IL-1β, and IL-6

by Dinesh Prasad V Thanga Velu, Mh Busra Fauzi, Faizul Jaafar, Norfilza Mohd Mokhtar, Mohd Helmy Mokhtar and Adila A Hamid

Int. J. Mol. Sci. 2026, 27(11), 4722; https://doi.org/10.3390/ijms27114722 - 24 May 2026

Viewed by 563

Abstract

The colonic epithelial barrier is a multilayered defense system comprising the mucus layer, intestinal epithelial cells (IECs), and the underlying lamina propria. These components collectively maintain mucosal homeostasis and restrict microbial translocation. Disruption of this barrier is a hallmark of chronic intestinal inflammation particularly in IBDs, and is primarily driven by pro-inflammatory cytokines, such as TNF-α, IFN-γ, IL-1β, and IL-6. TNF-α and IFN-γ synergistically induce epithelial cell apoptosis and tight junction disassembly through mechanisms involving TNFR2 upregulation, myosin light chain kinase (MLCK) activation, and adherens junction destabilization. IL-1β amplifies paracellular permeability via NF-κB-dependent MLCK induction and OCLN downregulation, while IL-6 promotes barrier leakiness by upregulating CLDN-2 and sustaining self-reinforcing inflammatory loops that maintain chronic inflammation and impede epithelial repair. This leads to persistent immune-cell infiltration, chronic tight junction remodeling, and failure of barrier replenishment. Consequently, leaky colon facilitates microbial and antigen translocation into the lamina propria, further activating immune cells and perpetuating pro-inflammatory signaling. This review synthesizes current evidence and studies on the cooperative and self-reinforcing roles of pro-inflammatory cytokines, providing insight into the mechanisms underlying chronic intestinal barrier dysfunction and highlighting the need for therapeutic strategies that simultaneously target multiple inflammatory axes to restore barrier integrity in inflammatory bowel disorders. Full article

(This article belongs to the Special Issue Cytokines and Inflammatory Diseases)

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17 pages, 638 KB

Open AccessReview

Mast Cells Accumulate in the Stroma of Breast Adenocarcinoma and Secrete Pro-Inflammatory Cytokines and Tumor-Damaging Mediators: Could IL-37 and IL-38 Play an Anti-Tumor Role?

by Pio Conti, Carla E. Gallenga, Ciro Annicchiarico, Armando Coppola, Raffaello Pellegrino, Michelangelo J. Conti and Filiberto Mastrangelo

Int. J. Mol. Sci. 2026, 27(2), 824; https://doi.org/10.3390/ijms27020824 - 14 Jan 2026

Cited by 1 | Viewed by 825

Abstract

Tumor tissue is surrounded by mast cells (MCs), which participate in the inflammatory immune response by producing cytokines, proteases, and other molecules. MCs are involved in both innate and acquired immunity and are associated with the IgE response through the FcεRI receptor. MCs mediate inflammation in several immune reactions, including acute hyperreactivity, leukocyte recruitment, acute tissue swelling, anaphylaxis, and pro-inflammatory cytokine production. They not only function as pro-inflammatory effector cells but may also contribute to the regulation of the acquired immune response in tumor tissue. Therefore, MCs may mediate immunity in breast cancer by promoting remodelling and counteracting cancer growth. They also produce anti-inflammatory substances, such as histamine, transforming growth factor-β (TGF-β)1, IL-10, and IL-4, which inhibit the acquired immune response and reduce the inflammatory state. IL-37 and IL-38 are novel natural regulators of inflammation and are anti-inflammatory members of the IL-1 family. IL-1, generated by immune cells such as macrophages and lymphocytes, is released downstream of oncogenes in breast cancer, triggering an inflammatory response by stimulating other pro-inflammatory cytokines such as IL-6, tumor necrosis factor (TNF), and IL-33 (an early warning cytokine). Therefore, blocking IL-1 with IL-37 or IL-38 could represent a novel therapeutic strategy that, when combined with other treatments, could be beneficial in breast cancer. This review focuses on the new discoveries and insights into the role of MCs in breast cancer. We also analyzed molecules that can promote tumor growth and those that can inhibit cancer development and metastasis. This review aims to study the role of MCs accumulated in the stroma of breast adenocarcinoma in relation to secreted anti-inflammatory cytokines, such as IL-37 and IL-38. Full article

(This article belongs to the Special Issue Cytokines and Inflammatory Diseases)

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29 pages, 1499 KB

Open AccessReview

Multifaceted Roles of IL-26 in Physiological and Pathological Conditions

by Boryana Georgieva, Danijela Karanović, Ivona Veličković and Danail Minchev

Int. J. Mol. Sci. 2026, 27(1), 325; https://doi.org/10.3390/ijms27010325 - 28 Dec 2025

Cited by 1 | Viewed by 1409

Abstract

Cytokines are a diverse group of signaling proteins that regulate immune responses by mediating cell communication. Among them, interleukins (ILs) play essential roles in immune regulation, influencing diverse cell processes through tightly controlled signaling networks. Dysregulation of interleukin signaling could lead to chronic inflammation, contributing to the development of autoimmune and inflammatory diseases as well as cancer. IL-26, a cytokine of the IL-10 family, has emerged as a unique modulator of immune function. Although structurally related to IL-10 and sharing one of its receptor subunits, IL-26 exerts distinct biological effects, particularly in promoting inflammatory responses and interacting with extracellular DNA to activate immune pathways. Increasing evidence implicates IL-26 in the development of several chronic conditions, such as psoriasis, rheumatoid arthritis, inflammatory bowel disease, asthma, and various types of cancer. This review summarizes current knowledge on IL-26’s biology, including its structural and receptor characteristics, immunomodulatory functions, and roles in inflammation and disease. Understanding IL-26’s dual functions in normal and inflammatory states may provide insights into novel therapeutic strategies targeting IL-26-mediated pathways in pathological conditions. Full article

(This article belongs to the Special Issue Cytokines and Inflammatory Diseases)

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