ijms-logo

Journal Browser

Journal Browser

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: 31 December 2024 | Viewed by 754

Special Issue Editor


E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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

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

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

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.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

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
Viewed by 532
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)
Show Figures

Figure 1

Back to TopTop