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New Insights into Immune and Anti-inflammatory Strategies for Improving Human Health

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: 20 February 2025 | Viewed by 5078

Special Issue Editor

Dr. Nikolina Mihaylova

E-Mail Website
Guest Editor
Laboratory of Experimental Immunology, Institute of Microbiology, Bulgarian Academy of Sciences, 1113 Sofia, Bulgaria
Interests: autoimmunity; osteoarthritis; B cells; T cells; cell signaling; mouse models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is evolutionarily determined that the immune system copes with the harmful effects of viruses and bacteria, as well as the development of autoimmune and tumor processes. Managing these health challenges successfully relies on a multitude of distinct and specific cells, the complexity of immune system components (including innate, humoral, and cellular), and the interplay of complex genetic and environmental factors. The principles that control the immune response to infection manifest in many normal physiological processes and in autoimmunity, making them applicable to cancer treatment.

The current Special Issue will attempt to provide a comprehensive overview of recent developments in the field of immunology and inflammation management. Our goal is to organize a collection of cutting-edge research and expert perspectives (original research articles, short communications, and reviews) that shed light on innovative approaches for immune activation, modulation, and tolerance in the context of immune and anti-inflammatory therapies to improve human health.

Dr. Nikolina Mihaylova
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • inflammation
  • immunotherapy
  • autoimmune disease
  • cancer
  • immune activation
  • modulation
  • tolerance

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Published Papers (5 papers)

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Research

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13 pages, 1116 KiB  
Article
Early Anti-Drug Antibodies Predict Adalimumab Response in Juvenile Idiopathic Arthritis
by Bo-Han Huang, Jr-Lin Hsu, Hsin-Yi Huang, Jing-Long Huang, Kuo-Wei Yeh, Li-Chen Chen, Wen-I Lee, Tsung-Chieh Yao, Liang-Shiou Ou, Syh-Jae Lin, Kuan-Wen Su and Chao-Yi Wu
Int. J. Mol. Sci. 2025, 26(3), 1189; https://doi.org/10.3390/ijms26031189 - 30 Jan 2025
Viewed by 266
Abstract
Adalimumab, a TNF-alpha inhibitor, is approved to treat juvenile idiopathic arthritis (JIA), helping control disease activity and reduce flare frequency. This study aims to investigate predictors of treatment response, including anti-drug antibodies. We reviewed 65 JIA patients (mean age 10.47 ± 3.90 years; [...] Read more.
Adalimumab, a TNF-alpha inhibitor, is approved to treat juvenile idiopathic arthritis (JIA), helping control disease activity and reduce flare frequency. This study aims to investigate predictors of treatment response, including anti-drug antibodies. We reviewed 65 JIA patients (mean age 10.47 ± 3.90 years; 61.5% male) receiving adalimumab for an average of 2.64 ± 0.56 years, with demographics, laboratory parameters, therapeutic regimens, and treatment outcomes recorded. Disease status was evaluated using the Wallace criteria up to 36 months post-treatment initiation, and anti-adalimumab antibody levels were measured after 6 months of treatment. Enthesitis-related arthritis was the most common subtype (64.6%). Inactive disease status was achieved by 83.1% of patients, with 59.3% experiencing relapse. Detectable anti-adalimumab antibody at six months (p = 0.023) and temporomandibular joint (TMJ) involvement (p = 0.038) identified those less likely to achieve inactive disease. An antibody level cutoff of 7.426 ng/mL best predicted response (AUC = 0.808; p = 0.008), while high anti-adalimumab antibody levels after treatment (p = 0.032) and an injection intervals over two weeks (p = 0.042) were predictors of future flares. Our results highlight that the presence of anti-adalimumab antibodies six months after treatment is a risk factor for poor response to adalimumab therapy. Full article
(This article belongs to the Special Issue New Insights into Immune and Anti-inflammatory Strategies for Improving Human Health)
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23 pages, 29492 KiB  
Article
Suppression of Pathological Allergen-Specific B Cells by Protein-Engineered Molecules in a Mouse Model of Chronic House Dust Mite Allergy
by Nikola Ralchev, Silviya Bradyanova, Nikola Kerekov, Andrey Tchorbanov and Nikolina Mihaylova
Int. J. Mol. Sci. 2024, 25(24), 13661; https://doi.org/10.3390/ijms252413661 - 20 Dec 2024
Viewed by 573
Abstract
Der p1 is one of the major allergens causing house dust mite (HDM) allergy. Pathological Der p1-specific B cells play a key role in allergic inflammation as producers of allergen-specific antibodies. Crosslinking the inhibitory FcγRIIb with the B cell receptor triggers a high-affinity [...] Read more.
Der p1 is one of the major allergens causing house dust mite (HDM) allergy. Pathological Der p1-specific B cells play a key role in allergic inflammation as producers of allergen-specific antibodies. Crosslinking the inhibitory FcγRIIb with the B cell receptor triggers a high-affinity suppressive signal in B cells. Selective elimination of allergen-specific cells could potentially be achieved by administering chimeric molecules that combine, through protein engineering, the FcγRIIb-targeting monoclonal 2.4G2 antibody with the epitope-carrying Dp52–71 peptides from Der p1. We tested this hypothesis, in a chronic mouse model of HDM allergy induced in BalB/c mice, using FACS and ELISA assays, along with histopathological and correlational analyses. Dp52–71chimera treatment of HDM-challenged mice led to a decrease in serum anti-HDM IgG1 antibodies, a reduction in BALF β-hexosaminidase levels, a lowered number of SiglecFhigh CD11clow eosinophils, and an improved lung PAS score. Furthermore, we observed overexpression of FcγRIIb on the surface of CD19 cells in the lungs of HDM-challenged animals, which negatively correlated with the levels of lung alveolar macrophages, neutrophils, and BALF IL-13. Taken together, these results suggest that the use of FcγRIIb overexpression, combined with the expansion of chimeric protein technology to include more epitopes, could improve the outcome of inflammation. Full article
(This article belongs to the Special Issue New Insights into Immune and Anti-inflammatory Strategies for Improving Human Health)
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17 pages, 3450 KiB  
Article
Soy Protein and Safflower-Seed Oil Attenuate Inflammation and Immune Dysfunction in Rats with Hyperuricemia
by Yi-Fang Liu, Yi-Chen Wu, Yu Yang and Hui-Chen Lo
Int. J. Mol. Sci. 2024, 25(23), 12977; https://doi.org/10.3390/ijms252312977 - 3 Dec 2024
Viewed by 681
Abstract
A plant-based diet is considered a promising approach for managing hyperuricemia (HUA). This study examined the effects of soy protein and plant-based oils on HUA-induced inflammation and immune dysfunction. Male Wistar rats, induced with HUA using oxonic acid and uric acid (UA), were [...] Read more.
A plant-based diet is considered a promising approach for managing hyperuricemia (HUA). This study examined the effects of soy protein and plant-based oils on HUA-induced inflammation and immune dysfunction. Male Wistar rats, induced with HUA using oxonic acid and uric acid (UA), were fed casein or soy protein with palm or safflower oil (2 × 2 factorial design) for 8 weeks. HUA rats had lower serum albumin and T cell percentages in peripheral blood leukocytes (PBLs) and splenocytes, along with increased leukocyte counts and spleen weights, compared to healthy rats (p < 0.05). Soy protein improved HUA-induced reductions in albumin, while safflower-seed oil ameliorated reductions in albumin, plasma interleukin (IL)-4, and T-suppressor splenocytes, and mitigated elevated serum UA, plasma IL-6, and B leukocytes (two-way ANOVA, p < 0.05). In PBL, soy protein alleviated HUA-induced decreases in TNF-α, casein and palm oil increased IL-6, and casein further reduced IFN-γ production. Under Con A stimulation, casein and safflower-seed oil alleviated decreases in IL-6 and IL-10, respectively, while under LPS stimulation, casein further increased TNF-α production. In splenocytes, soy protein and safflower-seed oil reduced HUA-induced increases in TNF-α and increased IL-10, and safflower-seed oil increased IL-6 production. Under Con A stimulation, soy protein and safflower-seed oil reduced TNF-α and increased IL-10 production in splenocytes. The findings suggest that soy protein and safflower-seed oil may counteract HUA-related inflammation, alleviate monocyte activation, and enhance Th2 immune response in HUA. A plant-based diet rich in soy protein and safflower-seed oil may help manage HUA and associated inflammation and immune dysfunction. Full article
(This article belongs to the Special Issue New Insights into Immune and Anti-inflammatory Strategies for Improving Human Health)
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16 pages, 3876 KiB  
Article
Gene Expression and Metabolome Analysis Reveals Anti-Inflammatory Impacts of 11,17diHDoPE on PM10-Induced Mouse Lung Inflammation
by Uijin Kim, Dong-Hyuk Kim, Deok-Kun Oh, Ha Youn Shin and Choong Hwan Lee
Int. J. Mol. Sci. 2024, 25(10), 5360; https://doi.org/10.3390/ijms25105360 - 14 May 2024
Cited by 1 | Viewed by 1164
Abstract
Oxylipins, the metabolites of polyunsaturated fatty acids, are vital in regulating cell proliferation and inflammation. Among these oxylipins, specialized pro-resolving mediators notably contribute to inflammation resolution. Previously, we showed that the specialized pro-resolving mediators isomer 11,17dihydroxy docosapentaenoic acid (11,17diHDoPE) can be synthesized in [...] Read more.
Oxylipins, the metabolites of polyunsaturated fatty acids, are vital in regulating cell proliferation and inflammation. Among these oxylipins, specialized pro-resolving mediators notably contribute to inflammation resolution. Previously, we showed that the specialized pro-resolving mediators isomer 11,17dihydroxy docosapentaenoic acid (11,17diHDoPE) can be synthesized in bacterial cells and exhibits anti-inflammatory effects in mammalian cells. This study investigates the in vivo impact of 11,17diHDoPE in mice exposed to particulate matter 10 (PM10). Our results indicate that 11,17diHDoPE significantly mitigates PM10-induced lung inflammation in mice, as evidenced by reduced pro-inflammatory cytokines and pulmonary inflammation-related gene expression. Metabolomic analysis reveals that 11,17diHDoPE modulates inflammation-related metabolites such as threonine, 2-keto gluconic acid, butanoic acid, and methyl oleate in lung tissues. In addition, 11,17diHDoPE upregulates the LA-derived oxylipin pathway and downregulates arachidonic acid- and docosahexaenoic acid-derived oxylipin pathways in serum. Correlation analyses between gene expression and metabolite changes suggest that 11,17diHDoPE alleviates inflammation by interfering with macrophage differentiation. These findings underscore the in vivo role of 11,17diHDoPE in reducing pulmonary inflammation, highlighting its potential as a therapeutic agent for respiratory diseases. Full article
(This article belongs to the Special Issue New Insights into Immune and Anti-inflammatory Strategies for Improving Human Health)
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16 pages, 1410 KiB  
Review
Mitigating Vascular Inflammation by Mimicking AIBP Mechanisms: A New Therapeutic End for Atherosclerotic Cardiovascular Disease
by Jun-Dae Kim, Abhishek Jain and Longhou Fang
Int. J. Mol. Sci. 2024, 25(19), 10314; https://doi.org/10.3390/ijms251910314 - 25 Sep 2024
Viewed by 1254
Abstract
Atherosclerosis, characterized by the accumulation of lipoproteins and lipids within the vascular wall, underlies a heart attack, stroke, and peripheral artery disease. Endothelial inflammation is the primary component driving atherosclerosis, promoting leukocyte adhesion molecule expression (e.g., E-selectin), inducing chemokine secretion, reducing the production [...] Read more.
Atherosclerosis, characterized by the accumulation of lipoproteins and lipids within the vascular wall, underlies a heart attack, stroke, and peripheral artery disease. Endothelial inflammation is the primary component driving atherosclerosis, promoting leukocyte adhesion molecule expression (e.g., E-selectin), inducing chemokine secretion, reducing the production of nitric oxide (NO), and enhancing the thrombogenic potential. While current therapies, such as statins, colchicine, anti-IL1β, and sodium–glucose cotransporter 2 (SGLT2) inhibitors, target systemic inflammation, none of them addresses endothelial cell (EC) inflammation, a critical contributor to disease progression. Targeting endothelial inflammation is clinically significant because it can mitigate the root cause of atherosclerosis, potentially preventing disease progression, while reducing the side effects associated with broader anti-inflammatory treatments. Recent studies highlight the potential of the APOA1 binding protein (AIBP) to reduce systemic inflammation in mice. Furthermore, its mechanism of action also guides the design of a potential targeted therapy against a particular inflammatory signaling pathway. This review discusses the unique advantages of repressing vascular inflammation or enhancing vascular quiescence and the associated benefits of reducing thrombosis. This approach offers a promising avenue for more effective and targeted interventions to improve patient outcomes. Full article
(This article belongs to the Special Issue New Insights into Immune and Anti-inflammatory Strategies for Improving Human Health)
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