Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.5
5.2
Journals
Cells
Special Issues
Study on Immune Activity of Natural Products
share announcement

Study on Immune Activity of Natural Products

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 June 2026 | Viewed by 2938

Special Issue Editor

Prof. Dr. Xiu-Min Li

E-Mail Website
Guest Editor
1. Department of Pathology, Microbiology & Immunology, New York Medical College, Valhalla, NY 10595, USA
2. Department of Otolaryngology, New York Medical College, Valhalla, NY 10595, USA
3. Department of Dermatology, New York Medical College, Valhalla, NY 10595, USA
Interests: allergy; asthma; inflammation; immune disorders; mechanisms of the immune system; natural products; Traditional Chinese Medicine (TCM)

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to the Special Issue entitled “Study on Immune Activity of Natural Products”. The immune system plays a critical role in maintaining health and combating diseases, and natural products have long been a rich source of bioactive compounds with immunomodulatory potential. With the growing interest in harnessing natural products for therapeutic applications, this research area holds significant promise for advancing our understanding of immune regulation and developing novel treatments for immune-related disorders.

This Special Issue aims to gather cutting-edge research on the immune-modulating properties of natural products, including plant-derived compounds, marine extracts, and microbial metabolites. By focusing on the mechanisms, efficacy, and applications of these bioactive substances, this collection will contribute to the broader field of cellular and molecular immunology.

In this Special Issue, original research articles and comprehensive reviews are welcome. Research areas may include (but are not limited to) the following:

  • The immunomodulatory effects of natural products derived from plants, animals, and microorganisms;
  • Immunostimulatory or the immunosuppressive effects of bioactive compounds;
  • How natural products influence immune signaling pathways and immune cells;
  • The potential of natural compounds to modulate autoimmune responses and restore immune balance;
  • The anti-inflammatory properties of natural products;
  • The applications of natural products in autoimmune diseases, infections, and cancer immunotherapy.

We look forward to receiving your contributions.

Prof. Dr. Xiu-Min Li
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • natural products
  • bioactive compounds
  • immune activity
  • immunomodulation
  • inflammation
  • autoimmune diseases
  • immunotherapy
  • therapeutic potential

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 (3 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

16 pages, 2428 KB  
Article
A Small Molecule Compound, Berberine Reduces IgE but Not IgG Production via Promoting miRNA-34a-p53 Axis
by Michelle Carnazza, Madison Spears, Raj K. Tiwari, Jan Geliebter, Nan Yang and Xiu-Min Li
Cells 2025, 14(22), 1799; https://doi.org/10.3390/cells14221799 - 17 Nov 2025
Viewed by 548
Abstract
Current therapeutic strategies for IgE-mediated diseases are limited. The drawbacks include adverse reactions, ineffectiveness, and relapses. Natural compound berberine (BBR) may combat this therapeutic gap through sustained transcriptional regulation of IgE. Human tonsil cells were cultured in the presence or absence of BBR [...] Read more.
Current therapeutic strategies for IgE-mediated diseases are limited. The drawbacks include adverse reactions, ineffectiveness, and relapses. Natural compound berberine (BBR) may combat this therapeutic gap through sustained transcriptional regulation of IgE. Human tonsil cells were cultured in the presence or absence of BBR to establish dose-dependent effects on IgE, IgG, and cell viability. IgE-producing plasma cells (U266, IgE plasma cells) and IgG-producing plasma cells (ARH-77, IgG plasma cells) were used as surrogate cells to validate dose-dependent effects on IgE and IgG production, respectively. At 10 μg/mL BBR, cell viability and proliferation were determined, and cells were harvested for protein, RNA, and miRNA and analyzed by Western blot and qPCR. BBR treatment of human tonsil samples resulted in reduced IgE production (p < 0.001) with no effect on IgG levels or cell viability. BBR demonstrated sustained, dose-dependent inhibition of IgE production by IgE plasma cells (p < 0.001), without affecting IgG production by IgG plasma cells. There was no significant reduction in cell viability of either cell type. Proliferation was reduced in IgE plasma cells (p = 0.02), but not IgG plasma cells. Assessment of IgE regulation and cell cycle at the RNA level revealed that BBR reduced IgE heavy chain expression and CCND1 (p < 0.01), with increased the GADD45A expression of IgE plasma cells, only (p = 0.016). At the protein level, BBR increased p53 (p = 0.02) and CDKN1C (p = 0.03), and decreased CDK2 (p = 0.01) expression of IgE plasma cells, only. Investigation of miRNAs implicated in B cell and p53 regulation demonstrated increased p53 and GADD45A activator, miR-34a (p = 0.04). miRNAs that are present in IgE plasma cells allow for specific effects on B cells and cell cycle genes by BBR, that are not present in IgG plasma cells. A novel mechanism for specific suppression of IgE by BBR highlights miR-34a, involved in the p53 pathway and B cell development, and may be crucial to pathological IgE production. Full article
(This article belongs to the Special Issue Study on Immune Activity of Natural Products)
►▼ Show Figures

Figure 1

23 pages, 6946 KB  
Article
Ginsenoside Derivative AD-1 Suppresses Pathogenic Phenotypes of Rheumatoid Arthritis Fibroblast-like Synoviocytes by Modulating the PI3K/Akt Signaling Pathway
by Yuan Fu, Fangfang Li, Biao Cui, Zhongyu Zhou, Xizhu Fang, Shengnan Huang, Xingguo Quan, Yuqing Zhao and Dan Jin
Cells 2025, 14(20), 1625; https://doi.org/10.3390/cells14201625 - 18 Oct 2025
Viewed by 888
Abstract
Rheumatoid arthritis (RA) is a systemic autoimmune disorder marked by chronic inflammation of small synovial joints, with frequent extra-articular involvement of the skin and eyes. Prolonged methotrexate therapy for RA is often accompanied by serious side effects. Therefore, new drugs with less toxicity [...] Read more.
Rheumatoid arthritis (RA) is a systemic autoimmune disorder marked by chronic inflammation of small synovial joints, with frequent extra-articular involvement of the skin and eyes. Prolonged methotrexate therapy for RA is often accompanied by serious side effects. Therefore, new drugs with less toxicity and greater effectiveness need to be developed. The ginsenoside 20(R)-25-methoxyl-dammarane-3β,12β,20-triol (AD-1), purified from Panax ginseng berry, exhibits potent anti-inflammatory and anti-cancer activities. However, the pharmacological mechanism of AD-1 in RA remains unclear. This study explored the potential anti-RA effects of AD-1 using an integrative strategy that combined network pharmacology, molecular docking, molecular dynamics simulation, and in vitro pharmacological validation. Enrichment analyses of KEGG and GO terms based on network pharmacology pointed to the PI3K/Akt signaling axis as a key regulatory pathway modulated by AD-1. Molecular docking and dynamics simulations revealed that AD-1 may have a close interaction with PIK3R1 and AKT1, demonstrating a stabilizing effect. Then, after experimental verification using human rheumatoid arthritis fibroblasts (MH7A), it was found that AD-1 suppressed cell proliferation, migration, and invasion and promoted apoptosis. Subsequent analysis of the RABC databases revealed that PIK3R1 and AKT1 were upregulated in RA, while AD-1 reduces phosphorylation of PI3K and Akt. In conclusion, these findings indicate that AD-1 exerts its anti-RA action, at least in part, through modulation of the PI3K/Akt signaling pathway and induction of apoptosis in synovial cells. This study provides a basis and new strategies for the role of ginsenosides in the treatment of RA. Full article
(This article belongs to the Special Issue Study on Immune Activity of Natural Products)
►▼ Show Figures

Graphical abstract

18 pages, 4533 KB  
Article
Formyl Peptide Receptors 1 and 2: Essential for Immunomodulation of Crotoxin in Human Macrophages, Unrelated to Cellular Entry
by Luciana de Araújo Pimenta, Ellen Emi Kato, Ana Claudia Martins Sobral, Evandro Luiz Duarte, Maria Teresa Moura Lamy, Kerly Fernanda Mesquita Pasqualoto and Sandra Coccuzzo Sampaio
Cells 2025, 14(15), 1159; https://doi.org/10.3390/cells14151159 - 26 Jul 2025
Viewed by 1030
Abstract
Crotoxin (CTX), the main toxin in Crotalus durissus terrificus venom, is a heterodimeric complex known for its antitumoral, anti-inflammatory, and immunomodulatory properties. In macrophages, CTX stimulates energy metabolism, pro-inflammatory cytokines, superoxide production, and lipoxin A4 secretion while inhibiting macrophage spreading and phagocytosis. [...] Read more.
Crotoxin (CTX), the main toxin in Crotalus durissus terrificus venom, is a heterodimeric complex known for its antitumoral, anti-inflammatory, and immunomodulatory properties. In macrophages, CTX stimulates energy metabolism, pro-inflammatory cytokines, superoxide production, and lipoxin A4 secretion while inhibiting macrophage spreading and phagocytosis. These effects are completely blocked by Boc-2, a selective formyl peptide receptors (FPRs) antagonist. Despite the correlation between FPRs and CTX-mediated effects, their involvement in mediating CTX entry into macrophages remains unclear. This study aimed to investigate the involvement of FPRs in CTX entry into monocytes and macrophages. For this, THP-1 cells were silenced for FPRs or treated with Boc-2. Results demonstrated that FPR-related signaling pathways, which influence macrophage functions such as ROS release, phagocytosis, and spreading, were reduced in FPR-silenced cells. However, even in the absence of FPRs, CTX was efficiently internalized by macrophages. These findings suggest that FPRs are essential for the immunomodulatory effects of CTX, but are not involved in CTX internalization. Full article
(This article belongs to the Special Issue Study on Immune Activity of Natural Products)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop