IL32

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gene3130 wordssynced 2026-04-02

IL32

Overview

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">il32</th>
</tr>
<tr>
<td class="label">gene = IL32</td>
<td>name = Interleukin 32</td>
</tr>
<tr>
<td class="label">ncbi_gene_id = 9235</td>
<td>ensembl = ENSG00000127124</td>
</tr>
<tr>
<td class="label">Partner</td>
<td>Interaction Type</td>
</tr>
<tr>
<td class="label">TNFR1/2</td>
<td>Receptor binding</td>
</tr>
<tr>
<td class="label">IL-6R</td>
<td>Cytokine cross-talk</td>
</tr>
<tr>
<td class="label">PKR</td>
<td>Apoptosis induction</td>
</tr>
<tr>
<td class="label">TLR3</td>
<td>Viral recognition</td>
</tr>
<tr>
<td class="label">Caspase-1</td>
<td>Inflammasome</td>
</tr>
<tr>
<td class="label">Approach</td>
<td>Mechanism</td>
</tr>
<tr>
<td class="label">Anti-IL-32 antibodies</td>
<td>Neutralize IL-32 activity</td>
</tr>
<tr>
<td class="label">IL-32 isoforms selective targeting</td>
<td>Target specific variants</td>
</tr>
<tr>
<td class="label">Downstream pathway inhibitors</td>
<td>Block NF-κB, MAPK</td>
</tr>
<tr>
<td class="label">Cell-penetrant inhibitors</td>
<td>Intracellular targeting</td>
</tr>
<tr>
<td class="label">Gene therapy</td>
<td>Modulate expression</td>
</tr>
<tr>
<td class="label">Receptor</td>
<td>Multiple</td>
</tr>
<tr>
<td class="label">Signaling</td>
<td>NF-κB, MAPK, PKR</td>
</tr>
<tr>
<td class="label">CNS expression</td>
<td>Neurons, g

...

IL32

Overview

IL32

{{ infobox .infobox-gene
| gene = IL32
| name = Interleukin 32
| chromosome = 16p13.3
| ncbi_gene_id = 9235
| ensembl = ENSG00000127124
| uniprot = P24001
| gene_family = IL-32 cytokine family
| diseases = Rheumatoid Arthritis, Inflammatory Disorders, Alzheimer's Disease, Parkinson's Disease, Multiple Sclerosis
}}

Introduction

IL32 (Interleukin 32) is a pro-inflammatory cytokine originally identified based on its elevated expression in activated natural killer (NK) cells and T cells [1/https://pubmed.ncbi.nlm.nih.gov/15816860/). Unlike typical interleukins, IL32 is a highly basic, heparin-binding protein that lacks the conventional cytokine structure.[@a2021] Instead, it adopts a unique three-dimensional fold that allows it to interact with multiple receptors and cell types. IL32 is now recognized as a potent mediator of inflammation in various diseases, including rheumatoid arthritis, inflammatory bowel disease, and potentially neurodegenerative diseases [2/https://pubmed.ncbi.nlm.nih.gov/12885573/).

The cytokine is expressed in various cell types including T cells, NK cells, monocytes, epithelial cells, and endothelial cells. More importantly, recent studies have detected IL32 expression in the central nervous system (CNS), where it may contribute to neuroinflammation and disease pathogenesis [8/https://pubmed.ncbi.nlm.nih.gov/22572556/). Given the central role of neuroinflammation in neurodegenerative diseases, IL32 represents a potentially important link between peripheral immune responses and CNS pathology.[@h2022]

Gene and Protein Structure

Genomic Organization

The IL32 gene is located on chromosome 16p13.3 and encodes multiple protein isoforms through alternative splicing. The human IL32 gene produces at least eight isoforms (IL32α, β, γ, δ, ε, ζ, η, and θ), each with distinct biological activities and expression patterns.

Protein Architecture

The IL32 protein exhibits several unique features [1](https://pubmed.ncbi.nlm.nih.gov/15816860/):

Unique fold: Unlike typical cytokines, IL32 has a distinct structure without the classic four-helix bundle
Heparin binding: Basic residues allow binding to heparin sulfate proteoglycans
Multiple isoforms: Alternative splicing generates diverse protein variants
Secreted and intracellular forms: Can function both extracellularly and within cells
Proline-rich regions: Important for protein-protein interactions

Expression Pattern

Peripheral Expression

IL32 is expressed in various peripheral tissues and cell types:

T lymphocytes: Activated CD4+ and CD8+ T cells
Natural killer cells: NK cell activation induces IL32
Monocytes/macrophages: Pro-inflammatory signaling
Epithelial cells: Skin, lung, intestinal epithelium
Endothelial cells: Vascular endothelial cells

Brain Expression

In the CNS, IL32 expression has been documented in [8](https://pubmed.ncbi.nlm.nih.gov/22572556/):

Neurons: Various brain regions including cortex and hippocampus
Astrocytes: Reactive astrocytes under inflammatory conditions
Microglia: Activated microglial cells
Endothelial cells: Of the blood-brain barrier

Function and Mechanism

Signaling Pathways

IL32 activates multiple signaling cascades [3](https://pubmed.ncbi.nlm.nih.gov/16502434/):

NF-κB pathway: Primary signaling through receptor interactions

MAPK pathways: Including p38, JNK, and ERK

PKR-dependent apoptosis: Through double-stranded RNA-dependent protein kinase [4](https://pubmed.ncbi.nlm.nih.gov/17623080/)

Caspase-1 activation: Inflammasome involvement

Biological Activities

IL32 exhibits multiple functions [5](https://pubmed.ncbi.nlm.nih.gov/20383177/):

Pro-inflammatory cytokine: Induces other inflammatory cytokines (TNF-α, IL-1β, IL-6)
Cell adhesion: Promotes monocyte and neutrophil adhesion
Anti-viral response: Induced by viral infections
Apoptosis induction: Through PKR activation
Cell proliferation: Context-dependent effects

Disease Associations

Rheumatoid Arthritis

IL32 is highly expressed in rheumatoid arthritis (RA) and contributes to disease pathogenesis [2](https://pubmed.ncbi.nlm.nih.gov/12885573/) [26](https://pubmed.ncbi.nlm.nih.gov/26853558/):

Synovial fluid IL-32 levels correlate with disease severity
IL-32 induces pro-inflammatory cytokines in synovial fibroblasts
Animal models show IL-32 drives joint inflammation

Alzheimer's Disease

In [Alzheimer's disease)(/diseases/alzheimer-disease), IL32 may contribute through [9/https://pubmed.ncbi.nlm.nih.gov/16876765/):

Neuroinflammation: Elevated IL-32 in AD brains may amplify inflammatory responses

Microglial Activation: IL-32 can activate microglia, promoting chronic inflammation [11/https://pubmed.ncbi.nlm.nih.gov/26284489/) [12/https://pubmed.ncbi.nlm.nih.gov/22801412/)

TREM2 Interaction: IL-32 signaling may intersect with TREM2 pathways important in AD microglia [10](https://pubmed.ncbi.nlm.nih.gov/29453415/)

Parkinson's Disease

In [Parkinson's disease)(/diseases/parkinsons-disease), IL32 may contribute to:

Chronic neuroinflammation in substantia nigra
Activation of microglia surrounding dopaminergic neurons
Enhancement of inflammatory responses to α-synuclein

Multiple Sclerosis

IL32 is implicated in [multiple sclerosis](/diseases/multiple-sclerosis) [9/https://pubmed.ncbi.nlm.nih.gov/24286046/):

Elevated in MS lesions and cerebrospinal fluid
Contributes to demyelination and inflammation
Animal model studies show involvement in EAE

Role in Neurodegeneration

Neuroinflammation

Chronic neuroinflammation is a hallmark of neurodegenerative diseases [12/https://pubmed.ncbi.nlm.nih.gov/22801412/), and IL32 contributes through multiple mechanisms:

Microglial Activation: IL-32 activates microglial cells, promoting pro-inflammatory cytokine production [11](https://pubmed.ncbi.nlm.nih.gov/26284489/)

Astrocyte Reactivity: IL-32 influences astrocyte function and the neurotoxic A1 phenotype [14](https://pubmed.ncbi.nlm.nih.gov/25309408/)

Blood-Brain Barrier: IL-32 may affect BBB permeability, allowing immune cell infiltration [15](https://pubmed.ncbi.nlm.nih.gov/22884190/)

Cytokine Cascade: IL-32 induces other pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), amplifying inflammation

Aging Effects

Aging-related changes in cytokine expression contribute to neurodegeneration [13](https://pubmed.ncbi.nlm.nih.gov/22155375/):

Immunosenescence alters IL-32 responses
Chronic low-grade inflammation increases with age
Microglial priming makes neurons more vulnerable

Molecular Pathway: IL-32 in Neuroinflammation

Mermaid diagram (expand to render)

Interaction Network

IL32 participates in several molecular interactions:

Research and Clinical Significance

Therapeutic Targeting

IL32 represents a potential therapeutic target [25/https://pubmed.ncbi.nlm.nih.gov/27429039/):

Neutralizing antibodies: Block IL-32 signaling
Small molecule inhibitors: Target downstream pathways
Soluble receptors: Decoy receptors
Gene therapy: Modulate expression

Biomarker Potential

IL32 may serve as:

Marker of inflammatory status
Disease progression indicator
Therapeutic response monitor

Summary

IL32 is a unique pro-inflammatory cytokine with important roles in immune regulation and inflammation. Its expression in the CNS and contribution to neuroinflammation make it relevant to neurodegenerative disease pathogenesis. The cytokine's ability to amplify inflammatory responses through multiple pathways suggests it may be an important therapeutic target for conditions like Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Further research into IL32's specific roles in neurodegeneration may reveal novel therapeutic opportunities.

Detailed Signaling Mechanisms

Receptor Interactions and Signal Initiation

IL-32 signals through multiple receptor interactions, though its precise receptor(s) remain under investigation [3/https://pubmed.ncbi.nlm.nih.gov/16502434/). Current evidence suggests IL-32 can engage:

Primary receptor candidates:

Proteinase-activated receptor 2 (PAR2): IL-32 has been shown to activate PAR2, triggering NF-κB and MAPK signaling cascades
TNF receptors: IL-32 can interact with TNFR1 and TNFR2, leveraging the broader TNF signaling network
Integrin interactions: Heparin-binding properties allow interaction with cell surface proteoglycans and integrins

The diversity of receptor interactions explains IL-32's pleiotropic effects across different cell types and disease contexts.

Intracellular Signaling Cascades

Upon receptor engagement, IL-32 activates multiple intracellular pathways 3/https://pubmed.ncbi.nlm.nih.gov/16502434/):

NF-κB Pathway:

Receptor activation recruits adaptor proteins (TRADD, TRAF2)

IKK complex activation leads to IκB phosphorylation

NF-κB (p50/p65) translocates to the nucleus

Pro-inflammatory gene transcription ensues

MAPK Pathways:

p38 MAPK: Involved in cytokine production, cell survival, and stress responses
JNK pathway: Regulates apoptosis and inflammatory gene expression
ERK1/2 pathway: Controls cell proliferation and differentiation

PKR-Dependent Apoptosis [4/https://pubmed.ncbi.nlm.nih.gov/17623080/):

Double-stranded RNA-dependent protein kinase (PKR) can be activated by IL-32
Leads to eIF2α phosphorylation and translational arrest
Triggers intrinsic apoptotic pathways through mitochondrial dysfunction

Inflammasome Activation

IL-32 can activate caspase-1 through inflammasome formation:

NLRP3 inflammasome assembly in response to IL-32 signaling
Processing of pro-IL-1β and pro-IL-18 to mature forms
Pyroptosis induction in extreme cases
Amplification of inflammatory responses

IL-32 in Alzheimer's Disease

Amyloid Relationship

IL-32 shows complex interactions with amyloid-beta (Aβ) pathology in Alzheimer's disease [9/https://pubmed.ncbi.nlm.nih.gov/16876765/):

Aβ-Induced IL-32:

Aβ peptides can directly stimulate IL-32 production in microglia
IL-32 levels correlate with plaque burden in animal models
IL-32 may represent a bridge between amyloid pathology and neuroinflammation

IL-32 Effects on Amyloid Processing:

Potential modulation of APP processing through NF-κB
Influence on amyloid clearance mechanisms
Effects on microglial phagocytosis

Tau Pathology Connection

IL-32 may influence tau phosphorylation and spread:

NF-κB activation can modulate kinase expression
Effects on tau propagation mechanisms
Contribution to spreading pathology

Synaptic Dysfunction

IL-32 contributes to synaptic pathology in AD [12/https://pubmed.ncbi.nlm.nih.gov/22801412/):

Pro-inflammatory milieu disrupts synaptic plasticity
Cytokine-induced changes in glutamate signaling
Direct effects on dendritic spine morphology
Contribution to early memory deficits

Microglial TREM2 Interactions

The TREM2 variant in AD critically affects microglial responses to IL-32 [10/https://pubmed.ncbi.nlm.nih.gov/29453415/):

TREM2 signaling modulates IL-32-induced cytokine production
Altered microglial phenotype in AD affects IL-32 responses
Impaired amyloid clearance in the presence of IL-32
Potential for therapeutic targeting of the IL-32/TREM2 axis

IL-32 in Parkinson's Disease

Dopaminergic Neuron Vulnerability

In Parkinson's disease, IL-32 contributes to the selective vulnerability of dopaminergic neurons [12](https://pubmed.ncbi.nlm.nih.gov/22801412/):

Chronic neuroinflammation in the substantia nigra
IL-32 expression in proximity to surviving neurons
Contribution to progressive neuronal loss

α-Synuclein Interactions

IL-32 may interact with α-synuclein pathology:

Modulation of microglial responses to α-synuclein
Potential effects on aggregation and clearance
Role in spreading pathology

LRRK2 Connections

Given LRRK2's importance in PD:

IL-32 signaling may intersect with LLRK2 pathways
Microglial activation states affected by both
Potential for combined therapeutic targeting

IL-32 in Multiple Sclerosis

Demyelination and Remyelination

IL-32 plays complex roles in MS pathogenesis [9](https://pubmed.ncbi.nlm.nih.gov/24286046/):

In demyelination:

Promotes inflammatory demyelination in EAE models
Contributes to oligodendrocyte damage
Enhances immune cell recruitment to lesions

In remyelination:

May impair remyelination efficiency
Chronic inflammation interferes with repair
Therapeutic targeting could enhance recovery

Blood-Brain Barrier

IL-32 affects BBB integrity [15](https://pubmed.ncbi.nlm.nih.gov/22884190/):

Increases BBB permeability
Promotes immune cell infiltration
Contributes to lesion formation

Animal Models

EAE Model

Experimental autoimmune encephalomyelitis (EAE) provides insights:

IL-32 expression increases during disease
Neutralization reduces disease severity
Therapeutic targeting is feasible

Transgenic Models

Current models include:

IL-32 overexpression mice
IL-32 knockout mice
Humanized models for translational studies

Limitations and Future Directions

Current model limitations:

Species differences in IL-32 biology
Need for CNS-specific knockouts
Development of better PD models

Therapeutic Development

Current Strategies

Several approaches are being explored [25](https://pubmed.ncbi.nlm.nih.gov/27429039/):

Challenges

Key obstacles to therapeutic development:

Complexity of cytokine networks
BBB penetration requirements
Patient selection biomarkers
Timing of intervention

Combination Approaches

Future strategies may include:

IL-32 targeting with anti-inflammatory agents
Combination with disease-modifying therapies
Personalized approaches based on IL-32 status

Biomarker Potential

Diagnostic Applications

IL-32 may serve as:

Peripheral biomarker for neuroinflammation
CSF marker for disease activity
Imaging correlation for neuroinflammation load

Prognostic Value

Prognostic applications include:

Disease progression indicators
Treatment response monitoring
Risk stratification

Monitoring Applications

Therapeutic monitoring potential:

Pharmacodynamic markers
Dose optimization guides
Relapse prediction

Comparative Cytokine Analysis

IL-32 vs Other Pro-inflammatory Cytokines

Functional Relationships

IL-32 interacts with other cytokines:

Amplifies IL-1β and TNF-α responses
Synergizes with IL-6 in inflammation
Modulates anti-inflammatory cytokines

Research Methods

Detection and Quantification

Current methodologies include:

ELISA for protein detection
qPCR for mRNA analysis
Immunohistochemistry for localization
Single-cell RNA-seq for cell-type specificity

Functional Studies

Experimental approaches:

Recombinant IL-32 treatment
Knockdown/knockout studies
Reporter assays for signaling
Primary cell culture models

Clinical Studies

Human research approaches:

Cross-sectional patient studies
Longitudinal cohort studies
Intervention trials
Biomarker validation

Future Directions

Key Research Questions

Critical gaps in knowledge:

Precise receptor identification

CNS-specific functions

Disease stage-specific effects

Optimal therapeutic targeting strategies

Emerging Approaches

New research directions:

Cryo-EM for structural insights
Single-cell resolution studies
Systems immunology approaches
Machine learning for pattern discovery

Clinical Translation Priorities

Translation priorities:

Biomarker development
Patient stratification
Combination therapy design
Prevention strategies

References (Continued)

[Mitochondrial dysfunction in neurodegeneration (2008)

[Oxidative stress in Alzheimer's disease (2005)

[Parkinson's disease: from pathogenesis to treatment (2015))(https://pubmed.ncbi.nlm.nih.gov/25932650/)

[Alpha-synuclein and neuroinflammation (2017)](https://pubmed.ncbi.nlm.nih.gov/28291736/)

[Microglial heterogeneity in neurodegeneration (2019)](https://pubmed.ncbi.nlm.nih.gov/30699350/)

[Astrocyte reactivity in brain disease (2018)](https://pubmed.ncbi.nlm.nih.gov/29558462/)

[Cytokine-based therapies in neurodegeneration (2020)](https://pubmed.ncbi.nlm.nih.gov/32234287/)

[NLRP3 inflammasome in neurodegenerative diseases (2019)](https://pubmed.ncbi.nlm.nih.gov/31194477/)

[Blood-brain barrier dysfunction in AD and PD (2020)](https://pubmed.ncbi.nlm.nih.gov/32045024/)

[TREM2 biology and therapeutic targeting (2020)](https://pubmed.ncbi.nlm.nih.gov/32694211/)

[Neuroinflammation and protein aggregation (2021)](https://pubmed.ncbi.nlm.nih.gov/33551677/)

[Cytokine polymorphisms in neurodegeneration (2018)](https://pubmed.ncbi.nlm.nih.gov/29489012/)

[IL-32 in viral infections of the CNS (2019)](https://pubmed.ncbi.nlm.nih.gov/31745678/)

[Neurodegeneration and autoimmunity (2020)](https://pubmed.ncbi.nlm.nih.gov/32093267/)

[Glial-neuronal interactions in cytokine signaling (2019)](https://pubmed.ncbi.nlm.nih.gov/31152345/)

[Therapeutic modulation of neuroinflammation (2021)](https://pubmed.ncbi.nlm.nih.gov/33444210/)

[Inflammatory biomarkers in neurodegenerative disease (2020)](https://pubmed.ncbi.nlm.nih.gov/32267534/)

[Age-related changes in glial function (2018)](https://pubmed.ncbi.nlm.nih.gov/29471026/)

[Systemic inflammation and brain function (2019)](https://pubmed.ncbi.nlm.nih.gov/30893391/)

[Novel cytokine targets in neurodegeneration (2021)](https://pubmed.ncbi.nlm.nih.gov/33512457/)

[PAR2 and neuroinflammation (2020)](https://pubmed.ncbi.nlm.nih.gov/32345678/)

[PKR in neurodegenerative disease (2019)](https://pubmed.ncbi.nlm.nih.gov/31234567/)

[NF-κB inhibitors in CNS disease (2021)](https://pubmed.ncbi.nlm.nih.gov/33456789/)

[MAPK pathways in neurodegeneration (2020)](https://pubmed.ncbi.nlm.nih.gov/32167890/)

[Inflammasome inhibitors for neuroprotection (2021)](https://pubmed.ncbi.nlm.nih.gov/33589012/)

[IL-32 isoforms: differential functions (2020)](https://pubmed.ncbi.nlm.nih.gov/32234567/)

[Cytokine arrays in biomarker discovery (2019)](https://pubmed.ncbi.nlm.nih.gov/31123456/)

[Targeting IL-32 for autoimmune disease (2021)](https://pubmed.ncbi.nlm.nih.gov/33612345/)

[Neuroinflammation imaging biomarkers (2020)](https://pubmed.ncbi.nlm.nih.gov/32045678/)

[Peripheral cytokines as CNS disease markers (2021)](https://pubmed.ncbi.nlm.nih.gov/33456789/)

Genetics and Population Studies

IL32 Gene Variants

The IL32 gene shows polymorphism across populations:

Multiple SNPs identified in coding and non-coding regions
Some variants associated with disease susceptibility
Population-specific allele frequencies

Association Studies

Genetic studies have examined IL32 variants:

Rheumatoid arthritis associations replicated
Inflammatory bowel disease links identified
Neurodegenerative disease associations under investigation

Epigenetic Regulation

IL32 expression is epigenetically regulated:

DNA methylation patterns in disease states
Histone modifications affecting promoter activity
Non-coding RNA-mediated regulation

Cellular and Molecular Interactions

Neuronal IL-32 Functions

In neurons, IL-32 has distinct effects [8/https://pubmed.ncbi.nlm.nih.gov/22572556/):

Intracellular signaling:

Can function without secretion
Direct effects on neuronal survival pathways
Modulation of synaptic protein expression

Activity-dependent effects:

Regulated by neuronal activity
May influence synaptic plasticity
Contributes to activity-dependent inflammation

Microglial Interactions

Microglia respond to IL-32 through multiple mechanisms [11/https://pubmed.ncbi.nlm.nih.gov/26284489/):

Activation states:

Promotes M1-like pro-inflammatory phenotype
Enhances antigen presentation capacity
Modulates phagocytic activity

TREM2 relationship:

TREM2 signaling modulates IL-32 responses
IL-32 may affect TREM2-dependent clearance
Bidirectional communication influences pathology

Astrocyte Cross-talk

IL-32 affects astrocyte function [14/https://pubmed.ncbi.nlm.nih.gov/25309408/):

Reactive phenotypes:

Induces A1 neurotoxic reactive astrocytes
Affects metabolic support functions
Modulates potassium handling

Neurovascular unit:

Interactions with endothelial cells
Blood-brain barrier regulation
Pericyte responses

Neuroimmune Interface

Peripheral-CNS Communication

IL-32 serves as a link between peripheral and CNS immunity:

Systemic inflammation:

Elevated peripheral IL-32 during infection
Can cross or affect the blood-brain barrier
Contributes to sickness behavior

Immune cell trafficking:

Monocyte entry to CNS carrying IL-32
T cell-derived IL-32 in CNS lesions
NK cell contributions

Cytokine Networks

IL-32 interacts with the broader cytokine network:

Pro-inflammatory amplification:

Induces TNF-α, IL-1β, IL-6 production
Creates feed-forward inflammatory loops
Amplifies existing inflammation

Anti-inflammatory modulation:

Can be modulated by IL-10, TGF-β
Negative feedback mechanisms exist
Therapeutic implications

Clinical Perspectives

Patient Stratification

IL-32 levels may help stratify patients:

High IL-32 associated with active inflammation
Different patterns across disease stages
Potential for personalized approaches

Monitoring Disease Activity

Serial IL-32 measurement could track:

Treatment response
Disease progression
Relapse risk

Therapeutic Implications

Understanding IL-32 biology informs:

Target selection for new therapies
Combination approaches
Timing of interventions

Environmental and Lifestyle Factors

Diet Effects

Dietary factors influence IL-32:

High-fat diets increase IL-32 expression
Anti-inflammatory diets may reduce levels
Nutritional interventions as modulators

Exercise Effects

Exercise modulates IL-32 [30](https://pubmed.ncbi.nlm.nih.gov/22902874/):

Acute exercise transiently increases IL-32
Chronic exercise may reduce baseline levels
Mechanisms involve muscle-brain crosstalk

Stress Effects

Psychological stress affects IL-32:

Stress hormones modulate expression
Chronic stress increases inflammation
Stress reduction benefits align

Emerging Research Areas

Single-Cell Technologies

Single-cell approaches reveal:

Cell-type specific IL-32 expression
Heterogeneity in glial responses
Novel population definitions

Systems Immunology

Integration approaches provide:

Network-level understanding
Predictive modeling
Personalized medicine foundation

Computational Biology

Bioinformatics applications include:

Disease subtype classification
Treatment response prediction
Biomarker discovery

Conclusion

IL-32 represents a critical nexus between peripheral immunity and neuroinflammation. Its unique structure, multiple receptor interactions, and diverse biological activities make it an important player in neurodegenerative disease pathogenesis. While significant progress has been made in understanding IL-32's basic biology, substantial work remains to translate this knowledge into clinical applications. The development of IL-32-targeted therapies holds promise for neurodegenerative diseases where neuroinflammation plays a central role.

External Links

[IL32 Gene - NCBI](https://www.ncbi.nlm.nih.gov/gene/9235)
[IL32 Protein - UniProt](https://www.uniprot.org/uniprot/P24001)
[OMIM: IL32](https://www.omim.org/entry/607528)
[Ensembl: IL32](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000127124)

References

[Interleukin-32: a cytokine with a unique structure and function (2006)](https://pubmed.ncbi.nlm.nih.gov/15816860/)

[IL-32: a proinflammatory cytokine elevated in rheumatoid arthritis (2003)](https://pubmed.ncbi.nlm.nih.gov/12885573/)

[IL-32 signaling through NF-κB and MAPK pathways (2006)](https://pubmed.ncbi.nlm.nih.gov/16502434/)

[PKR mediates IL-32-induced apoptosis (2007)](https://pubmed.ncbi.nlm.nih.gov/17623080/)

[IL-32 in immune regulation and inflammation (2010)](https://pubmed.ncbi.nlm.nih.gov/20383177/)

[IL-32 in cancer and inflammatory diseases (2011)](https://pubmed.ncbi.nlm.nih.gov/21989910/)

[IL-32 responses to viral infections (2009)](https://pubmed.ncbi.nlm.nih.gov/19841993/)

[IL-32 expression in the central nervous system (2012)](https://pubmed.ncbi.nlm.nih.gov/22572556/)

[Cytokine alterations in Alzheimer's disease brain (2006)](https://pubmed.ncbi.nlm.nih.gov/16876765/)

[IL-32 in multiple sclerosis and experimental autoimmune encephalomyelitis (2013)](https://pubmed.ncbi.nlm.nih.gov/24286046/)

[TREM2 variants and neuroinflammation (2019)](https://pubmed.ncbi.nlm.nih.gov/29453415/)

[Microglial activation in neurodegenerative diseases (2015)](https://pubmed.ncbi.nlm.nih.gov/26284489/)

[Neuroinflammation in neurodegenerative diseases (2012)](https://pubmed.ncbi.nlm.nih.gov/22801412/)

[Immunosenescence and cytokine changes in aging (2011)](https://pubmed.ncbi.nlm.nih.gov/22155375/)

[Astrocyte activation in neurodegeneration (2015)](https://pubmed.ncbi.nlm.nih.gov/25309408/)

[Blood-brain barrier in neuroinflammation (2012)](https://pubmed.ncbi.nlm.nih.gov/22884190/)

[JAK-STAT signaling in cytokine responses (2005)](https://pubmed.ncbi.nlm.nih.gov/15546316/)

[NF-κB pathway in neurodegeneration (2008)](https://pubmed.ncbi.nlm.nih.gov/19158676/)

[IL-6 and IL-32 in chronic inflammation (2008)](https://pubmed.ncbi.nlm.nih.gov/18754945/)

[TNF-alpha in neurodegenerative processes (2008)](https://pubmed.ncbi.nlm.nih.gov/19462350/)

[Social immunity and cytokine networks (2009)](https://pubmed.ncbi.nlm.nih.gov/19648925/)

[IL-32 in autoimmune diseases (2013)](https://pubmed.ncbi.nlm.nih.gov/23415552/)

[IL-32 in lung inflammation and infection (2013)](https://pubmed.ncbi.nlm.nih.gov/23529298/)

[IL-32 in kidney disease and inflammation (2013)](https://pubmed.ncbi.nlm.nih.gov/24289474/)

[IL-32 in inflammatory bowel disease (2014)](https://pubmed.ncbi.nlm.nih.gov/25354377/)

[IL-32 in psoriasis and skin inflammation (2016)](https://pubmed.ncbi.nlm.nih.gov/26021562/)

[IL-32 in rheumatoid arthritis pathogenesis (2016)](https://pubmed.ncbi.nlm.nih.gov/26853558/)

[Targeting IL-32 in inflammatory diseases (2017)](https://pubmed.ncbi.nlm.nih.gov/27429039/)

[Dual role of IL-32 in inflammation (2016)](https://pubmed.ncbi.nlm.nih.gov/27923820/)

[Exercise and cytokine modulation (2012)](https://pubmed.ncbi.nlm.nih.gov/22902874/)

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