Related Experiment Video

Updated: Jul 23, 2025

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors
04:59

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors

Published on: September 27, 2019

12.2K

IL-33/ST2 signaling in pain and itch: Cellular and molecular mechanisms and therapeutic potentials

Peiyi Li1, Qing Yu1, Huimin Nie1

  • 1Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|July 14, 2023
PubMed

Insights

Interleukin-33 (IL-33) and its receptor ST2 are implicated in chronic pain and itch. Targeting this pathway offers potential new treatments for these debilitating conditions.

Area of Science:

  • Immunology
  • Neuroscience
  • Pain Research

Background:

  • Chronic pain significantly impacts patients physically and mentally.
  • Current pain medications have limitations in efficacy and side effects.
  • Interleukin-33 (IL-33), part of the IL-1 cytokine family, binds to its receptor ST2.

Purpose of the Study:

  • To review the mechanisms of IL-33/ST2 signaling in pain and itch.
  • To explore potential similarities between IL-33/ST2's role in pain and itch.
  • To summarize clinical findings related to IL-33/ST2.

Main Methods:

  • Literature review of existing knowledge on IL-33/ST2 in pain and itch.
  • Analysis of studies investigating neuro-immune and neuron-glia crosstalk.
  • Inclusion of findings from relevant clinical studies.

Main Results:

  • IL-33/ST2 signaling regulates pain via neuroinflammation and neuronal hyperexcitability.
  • Emerging evidence links IL-33/ST2 signaling to chronic itch.
  • Clinical studies provide insights into the role of this pathway.

Conclusions:

  • IL-33/ST2 signaling is a key regulator in pain and itch conditions.
  • Targeting the IL-33/ST2 pathway presents a promising therapeutic strategy.
  • Novel treatments for chronic pain and itch may emerge from modulating IL-33/ST2.
Keywords:
GliaIL-33ItchNeuroinflammationNeuronPain

More Related Videos

Development of Recombinant Proteins to Treat Chronic Pain10:37

Development of Recombinant Proteins to Treat Chronic Pain

Published on: April 11, 2018

9.6K
Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 109:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

9.6K

Related Concept Videos

Analgesia and Pain Management01:25

Analgesia and Pain Management

Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
665
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.1K
Nociception01:44

Nociception

Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.
28.0K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.0K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.5K
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
2.2K