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Molecular Mechanisms and Therapeutic Targets in Inflammation and Cancer Immunity
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Molecular Mechanisms and Therapeutic Targets in Inflammation and Cancer Immunity

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: 31 October 2026 | Viewed by 2279

Editor

Dr. Hyuk Soon Kim

E-Mail Website
Guest Editor
Department of Biomedical Sciences, College of Natural Science, Dong-A University, Busan 49315, Republic of Korea
Interests: immune regulation; regulatory cells; innate lymphoid cells; allergy; atopic dermatitis; rheumatoid arthritis; autoimmune diseases; cancer; immune evasion; antibody-drug conjugation; chimeric antigen receptor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation and cancer immunity are intricately interconnected through a complex array of molecular pathways that regulate immune activation, suppression, and tissue homeostasis. Understanding these processes has become increasingly important for developing new approaches to managing chronic inflammatory diseases and maximizing the efficacy of immunotherapies in cancer. This Special Issue, “Molecular Mechanisms and Therapeutic Targets in Inflammation and Cancer Immunity,” aims to highlight recent progress in elucidating the molecular basis of immune regulation, inflammatory signaling, and tumor immune evasion. Topics include cytokine and chemokine networks, immune checkpoint modulation, antibody-based therapeutics, drug repositioning, and cellular or molecular mechanisms underlying immune tolerance. We welcome original research articles, reviews, and short communications focusing on the mechanistic and translational aspects of inflammation, immune regulation, and cancer immunology.

Dr. Hyuk Soon Kim
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-anonymized 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

  • immune regulation
  • inflammation
  • cancer immunity
  • immunotherapy
  • cytokine signaling
  • therapeutic targets
  • immune evasion
  • antibody-based therapy
  • histamine
  • drug repositioning

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Published Papers (2 papers)

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Review

26 pages, 7637 KB  
Review
Therapy-Driven Molecular Evolution of Bladder Cancer: Roles of Cellular Plasticity and Tumor Microenvironment
by Seung-Woo Baek, Seo-Young Yoon, Seon-Kyu Kim and Sun-Hee Leem
Int. J. Mol. Sci. 2026, 27(12), 5152; https://doi.org/10.3390/ijms27125152 - 6 Jun 2026
Viewed by 738
Abstract
Drug resistance remains a significant barrier to achieving durable treatment responses. Traditionally, resistance has been attributed to genetic alterations and clonal selection. However, accumulating evidence suggests that early adaptation to therapy is often mediated by non-genetic state transitions. In this review, we propose [...] Read more.
Drug resistance remains a significant barrier to achieving durable treatment responses. Traditionally, resistance has been attributed to genetic alterations and clonal selection. However, accumulating evidence suggests that early adaptation to therapy is often mediated by non-genetic state transitions. In this review, we propose a conceptual framework in which resistance emerges through therapy-driven molecular evolution in bladder cancer, characterized by three interconnected axes: non-genetic plasticity, metabolic reorganization, and tumor microenvironment remodeling. Using the Gemcitabine-Resistant Cell (GRC) model as a temporal reference system, we describe a stepwise transition from drug-sensitive states dominated by proliferation to survival-optimized resistant states through a growth–survival trade-off. Early adaptive phases are marked by the attenuation of cell-cycle and glycolytic programs, increased epigenetic flexibility, and metabolic rewiring involving mitochondrial and lipid-associated pathways. Later phases involve the reinforcement of resistance through extracellular matrix remodeling, developmental and stress-response signaling, and immunometabolic interactions within the tumor microenvironment, including adenosine- and lipid-associated mediators. Projecting the GRC score onto a clinical bladder cancer cohort further suggests that these evolutionary patterns may also be reflected in patient tumors. Overall, this framework supports a temporally structured view of chemoresistance and highlights opportunities to therapeutically target transitional adaptive states before resistance becomes stabilized. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Inflammation and Cancer Immunity)
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15 pages, 758 KB  
Review
Histamine-Mediated Syndrome (HMS): Beyond Allergy and Therapeutic Potential of Immunoglobulin/Histamine Complex (IHC)
by Hyuk Soon Kim and Geunwoong Noh
Int. J. Mol. Sci. 2026, 27(10), 4494; https://doi.org/10.3390/ijms27104494 - 17 May 2026
Viewed by 985
Abstract
Histamine, present in almost all tissues, exerts diverse biologic actions through four receptors expressed across multiple organs and cell types. Histamine concentrations are elevated in various conditions. A wide spectrum of clinical manifestations where histamine levels increase has been described. When plasma histamine [...] Read more.
Histamine, present in almost all tissues, exerts diverse biologic actions through four receptors expressed across multiple organs and cell types. Histamine concentrations are elevated in various conditions. A wide spectrum of clinical manifestations where histamine levels increase has been described. When plasma histamine concentrations are increased, multiple symptoms may occur via histamine receptor-mediated signaling. These clinical situations are defined as histamine-mediated syndrome (HMS). Recent reports describe the use of an immunoglobulin/histamine complex (IHC) to treat conditions beyond classical allergic diseases, such as allergic rhinitis (AR) and chronic urticaria (CU). Baseline plasma histamine levels in AR and CU can be higher than expected. This suggests histamine-driven comorbid manifestations in tissues and organs expressing histamine receptors. Accordingly, HMS may be more common in routine practice than is generally appreciated. IHC may represent a rational therapeutic option for HMS. In this review, we define HMS and integrate the available evidence to propose a systematic clinical framework. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Inflammation and Cancer Immunity)
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