Targeting IL-1R1–mediated neuroinflammation in central nervous system injury and disease

Priyanshu Srivastava, Anubhav Dubey*

Maharana Pratap College of Pharmacy, Kanpur, Uttar Pradesh, India

Refer this article

Priyanshu Srivastava, Anubhav Dubey, 2025. Targeting IL-1R1–mediated neuroinflammation in central nervous system injury and disease. Journal of medical pharmaceutical and allied sciences, V 15, I 1, Pages 07 – 18. Doi: https://doi.org/10.55522/jmpas.V15I1.7004.

ABSTRACT

The brain and spinal cord (CNS) was thought to be "immune privileged" for a long time, meaning that it neither caused nor was vulnerable to inflammation. In response to injury, infection, or illness, resident CNS cells produce inflammatory mediators, such as proinflammatory cytokines, prostaglandins, or free radicals, and complement. These hormones then trigger chemokines and adhesion molecules, attract immune cells, andOn the other hand, inflammatory mediators may play two roles: they might be harmful in the short term but helpfulin the long run.glial cells in activation. Due to its location at the "epicentre" of inflammatory signalling networks, the interleukin one transmitter type 1 (IL-1R1) plays crucial roles in how the immune system functions. One known aspect of the autoimmune reaction in the brain and spinal cord (CNS) after injury and disease is elevated levels of cytokines, such as IL-1, or neuroinflammation. The functions of IL-1R1 in the Brain cellular environment remain controversial despite the fact that IL-1/IL-1R1 signalling within the CNS has been the focus of numerous investigations. The path physiology of numerous CNS disease states, including Alzheimer's disease (AD), Parkinson's syndrome (PD), amyotrophic lateral sclerosis; (ALS), multiple sclerosis (MS), schizophrenia, and prion diseases, is unquestionably closely associated with the ongoing stimulation of the IL-1/IL-1R1 signalling pathway. Crucially An increasing amount of research indicates that in several animal models of the aforementioned CNS illnesses, inhibiting IL-1R1 signalling by pharmacological or genetically means results in decreased neurological inflammation and delayed progression of the disease. This paper aims to discuss recent developments in the cellular functions of IL-1R1 and to highlight important features that make IL-1R1 an attractive target for the creation of new disease-modifying therapies for various CNS diseases.

Keywords:

Interleukin-1, Interleukin-1 receptor type 1, Neuroinflammation, CNS diseases, Tracability, Brain injury.

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