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Advances in Pro-Inflammatory and Anti-Inflammatory Cytokines

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 August 2025 | Viewed by 2210

Special Issue Editor


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Guest Editor
Armed Forces Radiobiology Research Institute, Uniformed Services University of the Health Sciences, Bethesda, MD 20889-5648, USA
Interests: signal transduction; apoptosis; autophagy; cytokine/inflammation storm; acute radiation syndrome
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Special Issue Information

Dear Colleagues,

Over the past few years, research on pro-inflammatory and anti-inflammatory cytokines has tremendously furthered our understanding in the field of biology on a molecular level with disease progression. The balance between pro-inflammatory and anti-inflammatory cytokines contributes to homeostasis and maintenance of well-being. This has led to the potential new therapies, providing prophylactic or mitigative benefits to the treatment of complicated diseases. For example, using exosomes packed with cytokine(s) to correct certain metabolic problems or organ dysfunction has been published. A great deal of this progress is due to efforts that bridge across disciplines including molecular biology, biochemistry, pharmacology, and clinical medicine. The focus of this Special Issue is to bring together the most recent developments and state-of-the-art research studies to understand the molecular interaction between pro-inflammatory and anti-inflammatory cytokines and develop advanced prophylactics, mitigators, and therapies by managing the crosstalk of pro-inflammatory and anti-inflammatory cytokines. Original research articles, comprehensive reviews, and other article types are all welcome.

Suitable topics include, but are not limited to, the following:

  • Cell-based therapy;
  • Nanomedicine;
  • Drug development and mechanisms of drug action;
  • Innate and acquired immunity;
  • Microbe–host response.

Dr. Juliann G. Kiang
Guest Editor

Manuscript Submission Information

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Keywords

  • pro-inflammation cytokine
  • anti-inflammation cytokine
  • chemotherapy
  • radiotherapy
  • signal transduction
  • microbiome–host response
  • sepsis
  • bone marrow
  • GI
  • brain

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Published Papers (2 papers)

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Research

13 pages, 2577 KiB  
Article
Anti-IL-4, Anti-IL-17, and Anti-IFN-Gamma Activity in the Saliva of Amblyomma sculptum Ticks
by Helioswilton Sales-Campos, Chamberttan Souza Desidério, Rafael Obata Trevisan, Rodolfo Pessato Timóteo, Victor Hugo Palhares Flávio-Reis, Yago Marcos Pessoa-Gonçalves, Marcos Vinicius da Silva, Eliane Esteves, Thiago de Jesus Oliveira, Pedro Ismael da Silva Junior and Carlo José Freire Oliveira
Int. J. Mol. Sci. 2025, 26(10), 4734; https://doi.org/10.3390/ijms26104734 - 15 May 2025
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Abstract
The saliva of hematophagous arthropods, such as ticks and triatomines, contains bioactive ligands capable of modulating immune molecules, including cytokines. Cytokines play a critical role in immune regulation and have therapeutic relevance in inflammatory and immune-mediated diseases. Despite recent advances, identifying cytokine-binding molecules [...] Read more.
The saliva of hematophagous arthropods, such as ticks and triatomines, contains bioactive ligands capable of modulating immune molecules, including cytokines. Cytokines play a critical role in immune regulation and have therapeutic relevance in inflammatory and immune-mediated diseases. Despite recent advances, identifying cytokine-binding molecules remains a significant challenge. Interferon-gamma (IFN-γ), interleukin-4 (IL-4), and interleukin-17 (IL-17) are key cytokines involved in inflammation, adaptive immunity, and host defense. This study evaluated the ability of salivary components from Amblyomma sculptum and compared the results to the triatomine Rhodnius neglectus (used as control) to bind to IL-2, IL-4, IL-6, IL-10, IL-17, IFN-γ, and TNF-α using ELISA assays with human cytokines. Saliva samples were tested at dilutions of 1:25, 1:50, and 1:100. Saliva from A. sculptum, which demonstrated significant anti-cytokine activity, was fractionated via HPLC to identify the active components. The results confirmed the inhibitory capacity of A. sculptum saliva on IFN-γ, IL-4, and IL-17, with inhibition rates ranging from 30% to 70%, depending on the cytokine and dilution. No inhibitory activity was observed against IL-2, IL-6, IL-10, or TNF-α. These findings underscore the immunomodulatory role of A. sculptum saliva during tick feeding and suggest its potential for the development of novel immunobiologics to treat inflammatory and immune-mediated diseases. Full article
(This article belongs to the Special Issue Advances in Pro-Inflammatory and Anti-Inflammatory Cytokines)
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14 pages, 2444 KiB  
Article
RIPK2 Is Crucial for the Microglial Inflammatory Response to Bacterial Muramyl Dipeptide but Not to Lipopolysaccharide
by Changjun Yang, Maria Carolina Machado da Silva, John Aaron Howell, Jonathan Larochelle, Lei Liu, Rachel E. Gunraj, Antônio Carlos Pinheiro de Oliveira and Eduardo Candelario-Jalil
Int. J. Mol. Sci. 2024, 25(21), 11754; https://doi.org/10.3390/ijms252111754 - 1 Nov 2024
Cited by 1 | Viewed by 1577
Abstract
Receptor-interacting serine/threonine protein kinase 2 (RIPK2) is a kinase that is essential in modulating innate and adaptive immune responses. As a downstream signaling molecule for nucleotide-binding oligomerization domain 1 (NOD1), NOD2, and Toll-like receptors (TLRs), it is implicated in the signaling triggered by [...] Read more.
Receptor-interacting serine/threonine protein kinase 2 (RIPK2) is a kinase that is essential in modulating innate and adaptive immune responses. As a downstream signaling molecule for nucleotide-binding oligomerization domain 1 (NOD1), NOD2, and Toll-like receptors (TLRs), it is implicated in the signaling triggered by recognition of microbe-associated molecular patterns by NOD1/2 and TLRs. Upon activation of these innate immune receptors, RIPK2 mediates the release of pro-inflammatory factors by activating mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB). However, whether RIPK2 is essential for downstream inflammatory signaling following the activation of NOD1/2, TLRs, or both remains controversial. In this study, we examined the role of RIPK2 in NOD2- and TLR4-dependent signaling cascades following stimulation of microglial cells with bacterial muramyl dipeptide (MDP), a NOD2 agonist, or lipopolysaccharide (LPS), a TLR4 agonist. We utilized a highly specific proteolysis targeting chimera (PROTAC) molecule, GSK3728857A, and found dramatic degradation of RIPK2 in a concentration- and time-dependent manner. Importantly, the PROTAC completely abolished MDP-induced increases in iNOS and COX-2 protein levels and pro-inflammatory gene transcription of Nos2, Ptgs2, Il-1β, Tnfα, Il6, Ccl2, and Mmp9. However, increases in iNOS and COX-2 proteins and pro-inflammatory gene transcription induced by the TLR4 agonist, LPS, were only slightly attenuated with the GSK3728857A pretreatment. Further findings revealed that the RIPK2 PROTAC completely blocked the phosphorylation and activation of p65 NF-κB and p38 MAPK induced by MDP, but it had no effects on the phosphorylation of these two mediators triggered by LPS. Collectively, our findings strongly suggest that RIPK2 plays an essential role in the inflammatory responses of microglia to bacterial MDP but not to LPS. Full article
(This article belongs to the Special Issue Advances in Pro-Inflammatory and Anti-Inflammatory Cytokines)
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