Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
4.9
Journals
IJMS
Special Issues
Dialogue Between Inflammation and Immunity: From Mechanism to Therapy
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Dialogue Between Inflammation and Immunity: From Mechanism to Therapy

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 March 2026 | Viewed by 749

Special Issue Editor

Dr. Nikolina Mihaylova

E-Mail
Guest Editor
Laboratory of Immunohistochemistry and Immunopathology, Department of Immunology, The Stephan Angeloff 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,

The dynamic dialogue between inflammation and the immune system is essential for health and disease management. Inflammation is vital for pathogen clearance and tissue repair but can also contribute to chronic disease when dysregulated. The immune system orchestrates inflammation as a defensive mechanism to combat infections and tissue injury. The interplay between immune cells, cytokines, and signaling pathways governs the balance between protective and pathological inflammation.

Chronic inflammation underlies many autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS). Dysregulated cytokine production, loss of immune tolerance, and persistent activation of autoreactive lymphocytes drive tissue damage in these conditions. Inflammation is a key component of the tumor microenvironment, influencing cancer initiation, progression, and metastasis. Pro-inflammatory cytokines such as IL-6 and TNF-α promote tumor growth, angiogenesis, and immune evasion. In contrast, immune checkpoint pathways (e.g., PD-1/PD-L1) facilitate tumor-induced immunosuppression. The metabolic disorders and cardiovascular diseases are also supported by chronic inflammation.

A deeper understanding of the intricate mechanisms underlying the interplay between inflammation and immunity is vital for developing innovative treatments, paving the way for personalized and effective therapies in immune-related diseases.

This Special Issue will offer a collection of cutting-edge research articles or reviews that explore molecular crosstalk between inflammation and immunity, elucidate the mechanisms underlying their regulation, and discuss emerging therapeutic strategies aimed at modulating these interactions for clinical benefit.

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
  • immune activation
  • immunomodulation
  • tolerance
  • immunotherapy
  • autoimmune diseases
  • cancer

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

13 pages, 748 KB  
Article
Association Between Proinflammatory Cytokines IL-6 and TNF-Alpha, Psychological Stress and Chronic Spontaneous Urticaria Severity
by Liborija Lugović-Mihić, Maja Štrajtenberger, Matea Kuna, Blaženka Ladika-Davidović, Ema Barac and Maja Vilibić
Int. J. Mol. Sci. 2025, 26(21), 10384; https://doi.org/10.3390/ijms262110384 - 25 Oct 2025
Viewed by 217
Abstract
Chronic urticaria (CU), defined as the appearance of wheals/angioedema lasting ≥6 weeks, is often associated with psychological factors like stress. Stress-induced reactions involve the psychological–neuroendocrine–immunological network, which influences disease course/outcome and patient quality of life (QoL). With 46 participants (23 with CU and [...] Read more.
Chronic urticaria (CU), defined as the appearance of wheals/angioedema lasting ≥6 weeks, is often associated with psychological factors like stress. Stress-induced reactions involve the psychological–neuroendocrine–immunological network, which influences disease course/outcome and patient quality of life (QoL). With 46 participants (23 with CU and 23 healthy controls/HCs), this research examined the relationship between values of serum proinflammatory cytokines (IL-6 and TNF-α), stress indicators (cortisol levels, perceived stress level), and clinical chronic spontaneous urticaria (CSU) features (CSU severity/UAS, patient QoL). For CSU patients, significantly higher levels of IL-6 (p = 0.002) and TNF-α (p = 0.001) were recorded, as well as higher cortisol levels (p = 0.015) and a lower perception of stress/PSS (p < 0.001) than for HCs. CSU severity linearly and positively correlated with serum cortisol level (r = 0.463; p = 0.463) and impaired QoL (r = 0.715; p < 0.001). Additionally, impaired QoL correlated positively with perceived stress (r = 0.523; p = 0.010) and negatively with age (r = −0.529; p = 0.009). Also, IL-6 levels negatively correlated with perceived stress (r = −0.402; p = 0.006) linearly and moderately. The significant negative correlation between psychological stress and CU indicates that a comprehensive approach to treatment is necessary. Full article
(This article belongs to the Special Issue Dialogue Between Inflammation and Immunity: From Mechanism to Therapy)
►▼ Show Figures

Figure 1

12 pages, 1630 KB  
Article
HSP90 Inhibition Disrupts 27-Hydroxycholesterol-Induced Inflammatory Signaling in Monocytic Cells
by Jaesung Kim, Munju Kwon, Dongha Park, Nakyung Kang, Yonghae Son, Ninib Baryawno, Byoung Soo Kim, Sik Yoon, Sae-Ock Oh, Dongjun Lee and Koanhoi Kim
Int. J. Mol. Sci. 2025, 26(20), 9963; https://doi.org/10.3390/ijms26209963 - 13 Oct 2025
Viewed by 287
Abstract
27-Hydroxycholesterol (27OHChol), a cholesterol metabolite, induces inflammatory responses in monocytic cells and promotes their differentiation into mature dendritic cells. Here, we examined whether inhibition of heat shock protein 90 (HSP90) modulates these responses. Treatment with ganetespib, a selective HSP90 inhibitor, significantly reduced chemokine [...] Read more.
27-Hydroxycholesterol (27OHChol), a cholesterol metabolite, induces inflammatory responses in monocytic cells and promotes their differentiation into mature dendritic cells. Here, we examined whether inhibition of heat shock protein 90 (HSP90) modulates these responses. Treatment with ganetespib, a selective HSP90 inhibitor, significantly reduced chemokine CCL2 expression, lowering monocytic cell migration. It also suppressed matrix metalloproteinase-9 (MMP-9) expression and attenuated the lipopolysaccharide (LPS) response otherwise amplified by 27OHChol. Furthermore, ganetespib decreased mature dendritic cell markers (CD80, CD83, CD88) and restored endocytic activity, indicating a less activated state. These changes suggest that HSP90 regulates 27OHChol-induced pro-inflammatory activation via its client proteins. To explore this mechanism, we examined the phosphorylation status of signaling proteins. 27OHChol enhanced phosphorylation of Akt and its downstream targets, S6 and 4E-BP1 within the Akt/mTORC1 pathway. Ganetespib reduced total and phosphorylated Akt and 4E-BP1, and selectively inhibited S6 phosphorylation without altering total protein level. Collectively, these findings demonstrate that HSP90 inhibition by ganetespib mitigates 27OHChol-driven monocytic cell activation through suppression of the HSP90-Akt/mTORC1 axis. Targeting this pathway may provide a promising therapeutic strategy for metabolic inflammation associated with oxysterols. Full article
(This article belongs to the Special Issue Dialogue Between Inflammation and Immunity: From Mechanism to Therapy)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop