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The Role of Cytokines and Autoantibodies Against Cytokines in Health...
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The Role of Cytokines and Autoantibodies Against Cytokines in Health and Disease

A special issue of Immuno (ISSN 2673-5601). This special issue belongs to the section "Autoimmunity and Immunoregulation".

Deadline for manuscript submissions: closed (20 February 2026) | Viewed by 13452

Special Issue Editor

Prof. Dr. Juan Bautista De Sanctis

E-Mail Website
Guest Editor
Insitute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University, 77900 Olomouc, Czech Republic
Interests: inflammation; natural killer (NK) cells; immune response; metabolism; vaccines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cytokines are small proteins that play a vital role in regulating the growth, inhibition, and activity of various cells. Some serve as signals to activate functions of the immune system; others are involved in more open spectra, affecting different cells. Due to their beneficial effects, several pharmacological options have been designed to facilitate the treatment of various diseases. Antibodies against specific cytokines have been successfully used in therapy and can interfere with the inflammatory response, decreasing disease burden.

Conversely, autoantibodies targeting cytokines have also been identified; their role is considered significant, at least in the immune response. It is thought they may neutralize and inhibit the physiological function of the cytokine. It is plausible that additional autoantibodies against other cytokines other than those related to the immune response exist and affect other functions therein. Autoantibodies against cytokines have also been observed in healthy individuals, and their function remains ambiguous.

This Special Issue is intended to examine the functions of cytokines within various physiological and pathological contexts and address the role of autoantibodies targeting cytokines. Contributions exploring pharmacological methods for modulating cytokine effects, including delivery mechanisms and inhibitory strategies, are also encouraged. Submissions from both human and animal model studies are welcome.

You may choose our Joint Special Issue in IJMS.

Prof. Dr. Juan Bautista De Sanctis
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Immuno is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cytokine
  • autoantibodies
  • cytokine therapy
  • cytokine inhibition

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Published Papers (6 papers)

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Research

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14 pages, 1544 KB  
Article
Genetic Polymorphisms of IL6-174G/C, TNF-308G/A, and TNF-238G/A and Risk of Pleural Tuberculosis in Venezuelan Patients
by Zaida Araujo, Jacobus Henri de Waard, Mercedes Fernández-Mestre, Douglas Silva, Carmen Judith Serrano, Luis Adrián De Jesús-González, Juan Ernesto Lopez-Ramos and Bruno Rivas-Santiago
Immuno 2026, 6(1), 4; https://doi.org/10.3390/immuno6010004 - 22 Dec 2025
Viewed by 710
Abstract
Tuberculosis (TB) has various clinical presentations; pulmonary TB (PTB) affects only the lungs, whereas extrapulmonary TB involves other organs, including pleural TB (PLTB). Immunological studies of patients with extrapulmonary TB primarily focus on the cellular Th1 response, which produces key cytokines, including IFN-γ, [...] Read more.
Tuberculosis (TB) has various clinical presentations; pulmonary TB (PTB) affects only the lungs, whereas extrapulmonary TB involves other organs, including pleural TB (PLTB). Immunological studies of patients with extrapulmonary TB primarily focus on the cellular Th1 response, which produces key cytokines, including IFN-γ, TNF, IL-12, and IL-6. TNF and IL-6 play functional roles in host resistance to Mycobacterium tuberculosis (Mtb) infection. Findings suggest that TNF facilitates macrophage containment of Mtb, whereas IL-6 increases macrophage apoptosis induced by Mtb. Studies of the human genome have identified single-nucleotide polymorphisms (SNPs) in genes encoding cytokines associated with TB susceptibility. This study aimed to assess the potential of the IL6-174G/C (rs1800795), TNF-308G/A (rs1800629), and TNF-238G/A (rs361525) SNPs as genetic biomarkers of susceptibility to PLTB in the Venezuelan mestizo population. A total of 269 individuals were included: 69 patients with PLTB and 200 healthy individuals. The IL6-174G/C, TNF-308G/A, and TNF-238G/A polymorphisms were determined by sequence-specific primer polymerase chain reaction (SSP-PCR). Results showed significantly higher frequencies of the G/C, G/A, and G/A genotypes in patients with PLTB (94.0%, 94.2%, and 83.3%) than in controls (40.0%, 19.0%, and 13.4%) for the IL6-174G/C, TNF-308G/A, and TNF-238G/A polymorphisms, respectively. Logistic regression analysis showed significant associations between the G/C, G/A, and G/A genotypes and susceptibility to PLTB. The IL6-174G/C, TNF-308G/A, and TNF-238G/A gene polymorphisms may serve as genetic biomarkers of susceptibility to PLTB in the Venezuelan mestizo population. Full article
(This article belongs to the Special Issue The Role of Cytokines and Autoantibodies Against Cytokines in Health and Disease)
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13 pages, 6438 KB  
Article
IFN-τ Modulates PBMC Cytokine Profile and T Cell Phenotype to Improve Endometrial Immune Composition in the Implantation Window: A Combined In Vitro and In Vivo Study
by Margarita Ruseva, Dimitar Parvanov, Rumiana Ganeva, Maria Handzhiyska, Jinahn Safir, Dimitar Metodiev, Georgi Stamenov and Savina Hadjidekova
Immuno 2025, 5(4), 51; https://doi.org/10.3390/immuno5040051 - 24 Oct 2025
Cited by 1 | Viewed by 1252
Abstract
Embryo implantation requires a finely tuned immune balance at the maternal–fetal interface. Interferon tau (IFN-τ), a key immunomodulator in ruminant implantation, may have therapeutic potential in human reproduction. This study investigated its effects on peripheral blood mononuclear cells (PBMCs) in vitro and the [...] Read more.
Embryo implantation requires a finely tuned immune balance at the maternal–fetal interface. Interferon tau (IFN-τ), a key immunomodulator in ruminant implantation, may have therapeutic potential in human reproduction. This study investigated its effects on peripheral blood mononuclear cells (PBMCs) in vitro and the subsequent impact on endometrial immune composition following intrauterine administration of these cells. The work was conducted in two stages. First, in vitro assays were performed with PBMCs from 20 patients with recurrent implantation failure (RIF) cultured with or without IFN-τ for 24 h. Cytokines (IL-10, IL-4, TNF-α, IL-6) were measured by ELISA, and T cell subsets (Th, cytT, Th1, Th2, Th9, Tfh, Th17, Treg) were analyzed by flow cytometry. IFN-τ increased IL-4 and reduced TNF-α and IL-6, indicating a Th2 profile shift. T-cell analysis revealed fewer cytT, Th1, Th9, and Th17 cells, more Th2 cells, and improved Th/Tk, Th1/Th2, and Th17/Treg ratios after IFN-τ. A second clinical study included 55 RIF patients who received intrauterine IFN-τ-modulated PBMCs. Post-treatment endometrial biopsies revealed more helper T cells and macrophages, with higher Th/total T, Th/cytT, and Th/macrophage ratios, suggesting a tolerogenic environment. Overall, IFN-τ modulates PBMCs in vitro and promotes a favorable endometrial immune profile in vivo, highlighting its potential as an immunotherapy in assisted reproduction. Full article
(This article belongs to the Special Issue The Role of Cytokines and Autoantibodies Against Cytokines in Health and Disease)
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20 pages, 10077 KB  
Article
Myostatin Regulates Inflammatory Cytokine and Chemokine Expression, Rheumatoid Arthritis Synovial Fibroblast Invasion, and CD4+ Th Cell Transmigration
by Samudra Lansakara, Janis Weis, Chathura Siriwardhana and Yongsoo Kim
Immuno 2025, 5(3), 42; https://doi.org/10.3390/immuno5030042 - 19 Sep 2025
Cited by 1 | Viewed by 1439
Abstract
Rheumatoid arthritis synovial fibroblasts (RASFs) play a pivotal role in joint destruction in RA. Myostatin (MSTN), a myokine, is highly expressed in the RA synovium; however, its role in the function of RASFs is unclear. We hypothesized that MSTN amplifies inflammatory cytokines/chemokines, promotes [...] Read more.
Rheumatoid arthritis synovial fibroblasts (RASFs) play a pivotal role in joint destruction in RA. Myostatin (MSTN), a myokine, is highly expressed in the RA synovium; however, its role in the function of RASFs is unclear. We hypothesized that MSTN amplifies inflammatory cytokines/chemokines, promotes RASF invasion, and facilitates CD4+ Th cell transmigration. Immortalized MH7A cells (RASFs) and healthy synovial fibroblasts (HSFs) were treated with MSTN (0, 10, 20 ng/mL) for 0, 24, and 48 h. Cytokines (IL-8, IL-17, TNF-α, IL-6, IL-23, IFN-γ, IFN-β) and chemokines (CCL2, CCL20, CXCL13, CXCL1) were quantified by ELISA, RT-qPCR, and Western blotting. To evaluate MSTN regulation, cells were treated with pro-inflammatory mediators (TNF-α, IL-17, IFN-γ, IFN-β, CCL2, CXCL1). MSTN’s effects on Thy-1(CD90)+ RASF/HSF proliferation, RASF invasion, and CD4+ T-cell transmigration were assessed. Compared with HSFs, RASFs exhibited greater proliferative activity. MSTN significantly upregulated cytokines/chemokines, with CXCL1 showing the strongest induction in RASFs. IFN-γ and IL-17 robustly increased MSTN expression, indicating a feed-forward loop. MSTN did not alter Thy-1(CD90)+ fibroblast proliferation but significantly enhanced RASF invasion and CD4+ T-cell transmigration. Neutralizing CXCL1 or IL-17 reduced transmigration, with stronger inhibition via CXCL1. These findings offer new insights into the role of MSTN in RA pathogenesis and highlight its potential as a therapeutic target. Full article
(This article belongs to the Special Issue The Role of Cytokines and Autoantibodies Against Cytokines in Health and Disease)
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Review

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20 pages, 1185 KB  
Review
Molecular Programming of Stem-Cell Differentiation: From Soluble Factors to Agonist Antibodies
by Hyukmin In and Kyung Ho Han
Immuno 2026, 6(1), 11; https://doi.org/10.3390/immuno6010011 - 31 Jan 2026
Viewed by 845
Abstract
Stem-cell differentiation technologies have traditionally relied on recombinant growth factors, cytokines, and morphogens to initiate and guide lineage specification toward clinically relevant cell types. These approaches have enabled substantial progress in regenerative medicine, as exemplified by recent advances in cell-replacement therapies for Parkinson’s [...] Read more.
Stem-cell differentiation technologies have traditionally relied on recombinant growth factors, cytokines, and morphogens to initiate and guide lineage specification toward clinically relevant cell types. These approaches have enabled substantial progress in regenerative medicine, as exemplified by recent advances in cell-replacement therapies for Parkinson’s disease, type 1 diabetes, and retinal degeneration. However, protein-based ligands and soluble factors are often limited by short half-lives, pleiotropic signaling, condition-dependent effects, and challenges in achieving precise spatial and temporal control in scalable systems. In this review, we survey differentiation strategies driven by administered substances, organizing the field into five material-centric modules: recombinant growth factors, cytokines, morphogens, exogenous ligands, and agonist antibodies. For each module, we summarize mechanistic principles, representative studies, controllable variables, and translational considerations. While growth factors, cytokines, morphogens, and exogenous ligands remain central tools for directing lineage commitment and maturation, recent studies indicate that agonist antibodies offer an additional and distinct means of controlling differentiation outcomes. These antibodies can function as receptor agonists while also imparting tissue-selective effects, enabling lineage specification with coordinated spatial targeting. By focusing on differentiation methods driven by administered molecules and excluding direct physical stimulation or complex 3D constructs, this review provides a framework that is particularly relevant to immunology and translational practice. We highlight agonist antibody-based induction as an emerging strategy that complements established ligand-based approaches and may broaden the design space for clinically applicable stem-cell differentiation. Full article
(This article belongs to the Special Issue The Role of Cytokines and Autoantibodies Against Cytokines in Health and Disease)
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23 pages, 2184 KB  
Review
Role of Inflammatory Mediators in Chronic Obstructive Pulmonary Disease Pathogenesis: Updates and Perspectives
by Pankush, Khushboo Bharti, Rohit Pandey, Namita Srivastava, Shashank Kashyap, Deepak Kumar, Lokender Kumar, Sunil K. Suman and Sanjay K. S. Patel
Immuno 2025, 5(2), 13; https://doi.org/10.3390/immuno5020013 - 15 Apr 2025
Cited by 3 | Viewed by 8055
Abstract
Chronic obstructive pulmonary disease (COPD) is a chronic, debilitating condition that affects the lungs and airways. It is characterized by persistent bronchitis, a condition exemplified by the inflammation of the bronchial tubes, the hypersecretion of mucus, emphysema, and the destruction of the airway [...] Read more.
Chronic obstructive pulmonary disease (COPD) is a chronic, debilitating condition that affects the lungs and airways. It is characterized by persistent bronchitis, a condition exemplified by the inflammation of the bronchial tubes, the hypersecretion of mucus, emphysema, and the destruction of the airway parenchyma. The combination of these conditions leads to persistent tissue damage, pulmonary fibrosis, and ongoing inflammation of the airways. The inflammatory response in COPD is a complex process that is orchestrated by a wide range of immune cells. These include lung epithelial cells, monocytes, macrophages, neutrophils, eosinophils, and T and B lymphocytes, among others. These cells work together to produce a wide range of inflammatory biomarkers that are involved in the pathogenesis of COPD. Some of the key inflammatory biomarkers that have been identified in COPD include a variety of cytokines, the C-reactive protein/serum albumin ratio, fibrinogen, soluble receptor for advanced glycation endproducts, club/clara cells in the lungs with a molecular weight of 16 kDa, surfactant protein D, adiponectin, reactive oxygen species, and proteases. This review aims to provide a comprehensive overview of the role of immune cells and key inflammatory biomarkers in the development and progression of COPD. It will delve into the intricacies of the inflammatory response in COPD, exploring the various cell types and biomarkers that are involved in this process. By understanding the underlying mechanisms that drive COPD, we can better develop targeted treatments that can help to alleviate the symptoms of COPD. Full article
(This article belongs to the Special Issue The Role of Cytokines and Autoantibodies Against Cytokines in Health and Disease)
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Other

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10 pages, 844 KB  
Case Report
Cytokine Release Syndrome-like Reactions Following Exposure to Iodinated Contrast Media: A Case Series
by Xin Rong Lim, Samuel Shang Ming Lee, Justina Wei-Lynn Tan, Sze-Chin Tan and Bernard Pui Lam Leung
Immuno 2026, 6(2), 25; https://doi.org/10.3390/immuno6020025 - 7 Apr 2026
Viewed by 352
Abstract
Hypersensitivity reactions to iodinated contrast media (ICM) are traditionally categorized as immediate or delayed reactions, involving IgE-mediated pathways, non–IgE-dependent mast cell or complement activation, or T cell–mediated immune mechanisms. However, we observed that some individuals develop systemic inflammatory responses that do not fit [...] Read more.
Hypersensitivity reactions to iodinated contrast media (ICM) are traditionally categorized as immediate or delayed reactions, involving IgE-mediated pathways, non–IgE-dependent mast cell or complement activation, or T cell–mediated immune mechanisms. However, we observed that some individuals develop systemic inflammatory responses that do not fit these established categories. We describe here a case series of three patients who developed cytokine release syndrome (CRS)-like reactions following iodinated contrast administration, which were initially difficult to distinguish from sepsis and were only recognized after recurrent episodes. Clinical presentation, laboratory findings, cytokine profiles, allergy investigations, and treatment outcomes were reviewed. All patients developed fever, rigors, and hypotension within 5 to 70 h after exposure, accompanied by leukocytosis and markedly elevated inflammatory markers despite negative microbiological investigations. Serum tryptase levels remained within the normal range with no significant rise, while cytokine analyses demonstrated elevations of pro-inflammatory interleukin-6 and other cytokines in patients 1 and 3 where samples were available. Standard corticosteroid premedication did not prevent recurrence, and one patient developed systemic symptoms following intradermal testing. All patients improved with high-dose systemic corticosteroids and supportive care. These findings suggest that ICM may induce a cytokine-mediated inflammatory phenotype distinct from classical hypersensitivity reactions, highlighting the importance of early clinical recognition to guide diagnosis and management. Full article
(This article belongs to the Special Issue The Role of Cytokines and Autoantibodies Against Cytokines in Health and Disease)
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