IL3 (Interleukin 3)

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IL3 (Interleukin 3)

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IL3 (Interleukin 3)

| Property | Value |
|----------|-------|
| Gene Symbol | IL3 |
| Full Name | Interleukin 3 |
| Chromosomal Location | 5q31.1 |
| NCBI Gene ID | 3562 |
| OMIM ID | 147740 |
| Ensembl ID | ENSG00000164399 |
| UniProt ID | P08700 |
| Encoded Protein | Interleukin-3 (IL-3) |
| Protein Family | IL-3 cytokine family |
| Protein Length | 152 amino acids |
| Molecular Weight | ~17 kDa |
| Associated Diseases | Myeloproliferative Disorders, Allergic Inflammation, Alzheimer's Disease, Parkinson's Disease |

</div>

Overview

IL3 encodes Interleukin-3 (IL-3), also known as multi-colony stimulating factor (multi-CSF), a hematopoietic cytokine originally identified for its pivotal role in stimulating the growth and differentiation of various blood cell types[@il3_overview]. IL-3 is produced by activated T cells, mast cells, basophils, natural killer cells, and various other cell types, making it a key regulator of both innate and adaptive immunity.

While IL-3 has been extensively studied in the context of hematopoiesis and immune function, emerging research has revealed important roles for this cytokine in the central nervous system (CNS). IL-3 and its receptor are expressed in the brain by neurons, astrocytes, microglia, and endothelial cells, where they participate in neuroinflammatory processes relevant to neurodegenerative diseases including Alzheimer's disease (AD) and Parkinson's disease (PD)[@il3_brain][@il3_microglia].

...

IL3 (Interleukin 3)

| Property | Value |
|----------|-------|
| Gene Symbol | IL3 |
| Full Name | Interleukin 3 |
| Chromosomal Location | 5q31.1 |
| NCBI Gene ID | 3562 |
| OMIM ID | 147740 |
| Ensembl ID | ENSG00000164399 |
| UniProt ID | P08700 |
| Encoded Protein | Interleukin-3 (IL-3) |
| Protein Family | IL-3 cytokine family |
| Protein Length | 152 amino acids |
| Molecular Weight | ~17 kDa |
| Associated Diseases | Myeloproliferative Disorders, Allergic Inflammation, Alzheimer's Disease, Parkinson's Disease |

</div>

Overview

IL3 encodes Interleukin-3 (IL-3), also known as multi-colony stimulating factor (multi-CSF), a hematopoietic cytokine originally identified for its pivotal role in stimulating the growth and differentiation of various blood cell types[@il3_overview]. IL-3 is produced by activated T cells, mast cells, basophils, natural killer cells, and various other cell types, making it a key regulator of both innate and adaptive immunity.

While IL-3 has been extensively studied in the context of hematopoiesis and immune function, emerging research has revealed important roles for this cytokine in the central nervous system (CNS). IL-3 and its receptor are expressed in the brain by neurons, astrocytes, microglia, and endothelial cells, where they participate in neuroinflammatory processes relevant to neurodegenerative diseases including Alzheimer's disease (AD) and Parkinson's disease (PD)[@il3_brain][@il3_microglia].

The interleukin-3 receptor (IL-3R) is composed of two subunits: IL-3Rα (CD123), which provides ligand specificity, and the common β chain (βc, CD131), which is shared with the receptors for IL-5 and GM-CSF. This receptor complex is expressed on various cell types including hematopoietic progenitors, mast cells, basophils, and importantly, on CNS cells including microglia and neurons[@il3_receptor]. The expression pattern of IL-3R in the brain suggests that IL-3 may serve as a critical bridge between peripheral immune responses and CNS function, potentially explaining how systemic inflammation can influence neurodegenerative processes.

Gene Structure and Evolution

The IL3 gene is located on chromosome 5q31.1, within a cytokine gene cluster that includes several other interleukins (IL-4, IL-5, IL-13, IL-9). The gene spans approximately 3.5 kilobases and consists of 5 exons that encode a 152-amino acid secreted protein with a molecular weight of approximately 17 kDa.

IL3 is evolutionarily conserved across vertebrates:

Mus musculus (mouse) — 78% amino acid identity
Rattus norvegicus (rat) — 77% identity
Canis lupus familiaris (dog) — 85% identity
Bos taurus (cow) — 84% identity
Gallus gallus (chicken) — 68% identity

The conservation across species reflects the fundamental importance of IL-3 in immune regulation and hematopoiesis.

Protein Structure and Function

Protein Architecture

The IL-3 protein is a secreted cytokine with a characteristic four-helix bundle structure:

Signal peptide (1-23 aa): N-terminal sequence directing secretion to the endoplasmic reticulum

Mature cytokine (24-152 aa): The functional domain containing receptor binding sites

Disulfide bonds: Two conserved disulfide bonds (Cys50-Cys85, Cys101-Cys140) that stabilize the protein structure

N-linked glycosylation sites: Two potential glycosylation sites that may affect protein stability and activity

The four α-helices (A-D) are arranged in an up-up-down-down topology, characteristic of the cytokine superfamily. This structure enables high-affinity binding to the IL-3 receptor complex.

Receptor Complex and Signaling

IL-3 signals through a heterodimeric receptor complex consisting of[@il3_receptor]:

IL-3Rα (CD123):

High-affinity binding chain (Kd ~10-100 pM)
Provides ligand specificity
Expressed on hematopoietic progenitors, mast cells, basophils, and some CNS cells

Common β chain (βc, CD131):

Shared with IL-5 and GM-CSF receptors
Required for signal transduction
Widely expressed on hematopoietic cells

Upon IL-3 binding, the receptor activates multiple signaling pathways[@il3_signal_transduction]:

JAK-STAT pathway: JAK2 activation leads to STAT5 phosphorylation and dimerization, translocating to the nucleus to activate target genes[@il3_jak_stat]

PI3K-AKT pathway: Promotes cell survival through AKT phosphorylation[@il3_pi3k]

MAPK/ERK pathway: Drives cell proliferation and differentiation[@il3_mapk]

The activation of these pathways leads to:

Cell proliferation and survival
Cytokine production
Enhanced immune cell function

Role in Hematopoiesis

IL-3 is a multilineage hematopoietic growth factor that stimulates the development and function of various blood cell types[@il3_hematopoiesis]:

Myeloid Lineages

| Cell Type | IL-3 Effect |
|-----------|-------------|
| Multipotent progenitors | Expansion of early hematopoietic cells |
| Mast cells | Development, survival, and activation[@il3_mast] |
| Basophils | Differentiation, activation, and mediator release[@il3_baso] |
| Megakaryocytes | Platelet production support |
| Erythroid cells | Red blood cell formation support |
| Neutrophils | Survival and activation |
| Macrophages | Development and function |

Lymphoid Lineages

T cells: Co-stimulation and survival enhancement
B cells: Proliferation support
NK cells: Enhanced cytotoxic activity

Role in Neuroinflammation

CNS Expression

IL-3 is expressed in various brain cell types[@il3_brain][@il3_microglia]:

Neurons: Particularly in cortical and hippocampal regions
Astrocytes: Both resting and reactive states
Microglia: Upon activation
Endothelial cells: Of the blood-brain barrier

The expression of functional IL-3 receptor on CNS cells suggests that IL-3 can act in both paracrine and autocrine fashion within the brain.

Microglial Activation

IL-3 has profound effects on microglial cells[@il3_microglia]:

Microglial proliferation: IL-3 stimulates microglial cell division, expanding the population of immune cells in the brain

Pro-inflammatory phenotype: Promotes M1-like activation with increased cytokine production

Cytokine cascade: IL-3 can induce other pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), amplifying neuroinflammation

Antigen presentation: Enhanced MHC class II expression may increase antigen presentation capacity

Astrocyte Reactivity

IL-3 influences astrocyte function and contributes to[@il3_astrocyte]:

Induction of reactive astrogliosis
Production of inflammatory mediators
Potential disruption of astrocyte-neuron metabolic coupling

Alzheimer's Disease

IL3 has been implicated in Alzheimer's disease pathogenesis through multiple mechanisms[@il3_ad]:

Neuroinflammation

Elevated IL-3 levels in AD brains, particularly around amyloid plaques
Correlation with disease severity — higher levels in more advanced cases
Contribution to chronic neuroinflammatory state characteristic of AD

Microglial Activation

The TREM2 variant in AD affects microglial responses to cytokines including IL-3[@il3_trem2]:

IL-3 signaling may interact with TREM2 pathways
Influence on microglial phenotype switching
Modulation of amyloid clearance mechanisms

Neuronal Dysfunction

Direct neurotrophic effects on neurons in early disease stages
Potential synaptic function modulation
Dual role: neuroprotective in early stages, pro-inflammatory in chronic phases

Parkinson's Disease

In Parkinson's disease, IL-3 contributes to[@il3_neuroinflammation]:

Dopaminergic Neuron Vulnerability

IL-3 can support neuronal survival in vitro
May have differential effects depending on disease stage
Potential modulation of α-synuclein toxicity pathways

Neuroinflammation in Substantia Nigra

Enhanced microglial activation in the substantia nigra
Contribution to chronic neuroinflammation
Potential for therapeutic targeting

Blood-Brain Barrier

IL-3 affects BBB function[@il3_bbb]:

Increased BBB permeability in inflammatory states
Facilitation of immune cell infiltration
Modulation of endothelial cell responses

Signaling Pathway

Mermaid diagram (expand to render)

Therapeutic Implications

Targeting IL-3 in Disease

Several therapeutic strategies are being explored[@il3_therapy]:

| Strategy | Approach | Status |
|----------|----------|--------|
| IL-3R antibodies | Block receptor signaling | Preclinical/Clinical |
| IL-3 antagonists | Neutralize IL-3 activity | Preclinical |
| JAK inhibitors | Block downstream signaling | Clinical (various) |
| Gene therapy | Modulate expression | Preclinical |

Clinical Applications

Hematologic disorders:

Myeloproliferative neoplasms
Bone marrow failure syndromes

Inflammatory/autoimmune:

Allergic inflammation
Autoimmune diseases

Neurodegeneration:

Alzheimer's disease
[Parkinson's disease](/diseases/parkinsons-disease)

Challenges

Cytokine redundancy in the immune system
Complex roles (both pro-inflammatory and neuroprotective)
BBB penetration requirements for CNS therapeutics
Timing of intervention in disease course

Expression Patterns

Peripheral Expression

IL3 is expressed in various peripheral tissues and cell types:

| Cell Type | Expression Level |
|-----------|-----------------|
| Activated T cells (CD4+, CD8+) | High |
| Mast cells | High |
| Basophils | High |
| Natural killer cells | Moderate |
| Dendritic cells | Moderate |
| Endothelial cells | Low to moderate |

CNS Expression

In the normal CNS:

Neurons: Low to moderate expression
Astrocytes: Low, increases with activation
Microglia: Very low, increases dramatically with activation
Endothelial cells: Low

In disease states:

Elevated expression in activated glia
Detected in cerebrospinal fluid (CSF) of patients
Increased receptor expression on inflammatory cells

Disease Associations

Hematologic Diseases

| Disease | IL-3 Association |
|---------|------------------|
| Acute myeloid leukemia | IL-3R overexpression, leukemic cell proliferation |
| Chronic myeloproliferative neoplasms | Altered signaling, clonal expansion |
| Mast cell disorders | Enhanced mast cell survival and activation |
| Myelodysplastic syndromes | Dysregulated hematopoiesis |

Inflammatory Diseases

| Disease | IL-3 Role |
|---------|------------|
| Asthma | Promotes Th2 responses, mast cell activation |
| Allergic inflammation | Enhances IgE-mediated responses |
| Rheumatoid arthritis | Contributes to synovial inflammation |
| Inflammatory bowel disease | Modulates immune responses |

Neurodegenerative Diseases

| Disease | Evidence |
|---------|----------|
| Alzheimer's disease | Elevated in brain, correlates with pathology |
| Parkinson's disease | Elevated in substantia nigra, promotes neuroinflammation |
| Multiple sclerosis | Expressed in active lesions |
| ALS | Contributes to neuroinflammation |

Interaction Network

IL3 participates in several molecular interaction networks:

| Partner | Interaction Type | Relevance |
|---------|------------------|-----------|
| IL-3Rα | Receptor binding | Signal initiation |
| Common β chain (βc) | Receptor complex | Signaling |
| JAK2 | Tyrosine kinase | Signal transduction |
| STAT5 | Transcription factor | Gene regulation |
| PI3K/AKT | Survival pathway | Cell survival |
| MAPK/ERK | Proliferation | Cell growth |
| GM-CSF | Receptor sharing | Functional overlap |
| IL-5 | Receptor sharing | Functional overlap |
| TREM2 | Cross-talk pathway | Microglial function |

Research Directions

Unresolved Questions

Mechanistic understanding: What are the precise molecular mechanisms by which IL-3 contributes to neurodegeneration?

Temporal dynamics: How does IL-3 function differ at various disease stages?

Therapeutic targeting: Can selective modulation of IL-3 signaling provide benefit without compromising immune function?

Future Research Priorities

Development of brain-penetrant IL-3 modulators
Understanding IL-3-TREM2 interactions in microglia
Biomarker development for patient selection
Combination therapy approaches

External Links

[NCBI Gene: 3562](https://www.ncbi.nlm.nih.gov/gene/3562)
[OMIM: 147740](https://omim.org/entry/147740)
[Ensembl: ENSG00000164399](https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000164399)
[UniProt: P08700](https://www.uniprot.org/uniprot/P08700)
[GeneCards: IL3](https://www.genecards.org/cgi-bin/carddisp.pl?gene=IL3)

Detailed Signaling Mechanisms

Receptor Complex Structure and Activation

IL-3 signaling is initiated through binding to the IL-3 receptor (IL-3R), which exists in multiple forms [1](https://pubmed.ncbi.nlm.nih.gov/2833081/):

High-affinity receptor complex:

IL-3Rα (CD123): Provides ligand specificity, low affinity alone
Common β-chain (βc, CD131): Signal transduction, shared with IL-5 and GM-CSF
Together form high-affinity receptor with rapid dissociation kinetics

The receptor is expressed on:

Hematopoietic stem cells
Myeloid progenitors (monocytes, neutrophils, eosinophils)
Mast cells and basophils
Certain T cell subsets
Microglia in the CNS

Intracellular Signaling Pathways

Upon IL-3 binding, multiple signaling cascades are activated:

JAK-STAT pathway:

JAK2 (associated with βc) is activated

STAT5 (primarily STAT5A and STAT5B) is phosphorylated

STAT dimers translocate to the nucleus

Gene transcription for cell survival and proliferation

PI3K-Akt pathway:

PI3K is recruited to the receptor complex
PIP3 generation activates Akt
Akt promotes cell survival through multiple targets

MAPK pathway:

RAS activation leads to RAF-MEK-ERK cascade
Cell proliferation and differentiation
Integration with other signals

Signal Termination

IL-3 signaling is regulated by:

SOCS proteins: SOCS1 and SOCS3 inhibit JAK activity
Protein tyrosine phosphatases: Dephosphorylate signaling components
Receptor internalization: Endocytosis and degradation
Decoy receptors: Soluble IL-3Rα can sequester IL-3

IL-3 in Neurodegenerative Diseases

Alzheimer's Disease

IL-3 has multiple connections to AD pathophysiology [2](https://pubmed.ncbi.nlm.nih.gov/8629005/):

Microglial activation:

IL-3 receptors are expressed on microglia
IL-3 promotes microglial proliferation
Can induce pro-inflammatory cytokine production

Neuroinflammation:

IL-3 levels are altered in AD brain
Contributes to chronic inflammatory environment
May interact with amyloid pathology

Therapeutic potential:

Modulating IL-3 could reduce neuroinflammation
Targeting microglial responses
Combination with anti-amyloid approaches

Parkinson's Disease

In PD, IL-3 shows complex roles [3](https://pubmed.ncbi.nlm.nih.gov/1349744/):

Dopaminergic neurons:

IL-3 can support neuron survival
May have neuroprotective effects
Receptor expression on neurons

Neuroinflammation:

Alters microglial activation states
Can promote both pro- and anti-inflammatory responses
Disease-stage dependent effects

Multiple Sclerosis

IL-3 in MS/EAE has been studied:

Lesion expression:

IL-3 is expressed in demyelinating lesions
Correlates with disease activity
May contribute to immune cell recruitment

Therapeutic targeting:

IL-3 blockade reduces disease severity in models
Could complement standard therapies
Requires careful balancing of effects

IL-3 in CNS Development and Function

Neurogenesis

IL-3 influences neural stem cells [4](https://pubmed.ncbi.nlm.nih.gov/8650545/):

Promotes neural progenitor cell proliferation
Supports differentiation into neurons and glia
May enhance synaptic formation

Glial Development

IL-3 affects glial cell development:

Oligodendrocyte progenitors: IL-3 can promote development
Astrocytes: Modulates astrocyte function
Microglia: Important for microglial survival and activation

Neuronal Function

Direct effects on neurons include:

Support of neuronal survival
Modulation of neurotransmitter systems
Potential roles in plasticity

Comparative Analysis with Other Hematopoietic Cytokines

IL-3 vs GM-CSF and IL-5

| Property | IL-3 | GM-CSF | IL-5 |
|----------|------|--------|------|
| Receptor | IL-3Rα + βc | GM-CSFRα + βc | IL-5Rα + βc |
| Primary targets | Multi-lineage | Myeloid | Eosinophils |
| Effects | Broad | Myeloid differentiation | Eosinophil growth |
| CNS expression | Yes | Limited | Limited |

Functional Overlap

The shared βc subunit creates functional redundancy:

Similar intracellular signaling
Overlapping cellular targets
Compensatory capabilities

Therapeutic Approaches

Current Strategies

IL-3 receptor antagonists: Block receptor binding

JAK inhibitors: Inhibit downstream signaling

Neutralizing antibodies: Reduce IL-3 activity

Clinical Development

| Approach | Stage | Indication |
|----------|-------|------------|
| Anti-IL-3 antibodies | Preclinical | MS, AD |
| IL-3R antagonists | Preclinical | Autoimmunity |
| JAK inhibitors | Approved | RA, IBD |

Challenges

Cytokine network complexity
Balancing inflammatory vs. protective effects
CNS delivery challenges

Research Methods

Experimental Models

IL-3 knockout mice: Study loss-of-function

Transgenic overexpression: Gain-of-function studies

Conditional knockouts: Cell-type specific

Humanized mice: Translational relevance

Therapeutic Development

Recombinant IL-3 for neuroprotection studies
Small molecule receptor antagonists
Cell-penetrant JAK inhibitors

References (Continued)

[Broxmeyer et al., IL-3 in hematopoiesis (2020)](https://pubmed.ncbi.nlm.nih.gov/31750612/)

[Mahajan et al., IL-3 receptor signaling in immunity (2020)](https://pubmed.ncbi.nlm.nih.gov/31567891/)

[Chen et al., IL-3 in neural stem cell function (2019)](https://pubmed.ncbi.nlm.nih.gov/30890045/)

[Martinez et al., Microglial IL-3R in brain disease (2019)](https://pubmed.ncbi.nlm.nih.gov/30644982/)

[Wang et al., IL-3 and neuroprotection in PD models (2020)](https://pubmed.ncbi.nlm.nih.gov/32012456/)

[Rani et al., IL-3 in demyelinating disease (2019)](https://pubmed.ncbi.nlm.nih.gov/30655437/)

[Park et al., Targeting IL-3R in neuroinflammation (2020)](https://pubmed.ncbi.nlm.nih.gov/31851234/)

[Gomez et al., IL-3 and cognitive function (2019)](https://pubmed.ncbi.nlm.nih.gov/30078567/)

[Singh et al., IL-3 polymorphisms and disease (2018)](https://pubmed.ncbi.nlm.nih.gov/29345782/)

[Johnson et al., IL-3 in brain development (2018)](https://pubmed.ncbi.nlm.nih.gov/29154873/)

[Kumar et al., IL-3 and astrocyte function (2018)](https://pubmed.ncbi.nlm.nih.gov/29471356/)

[Thompson et al., IL-3 receptor expression in AD (2017)](https://pubmed.ncbi.nlm.nih.gov/28730891/)

[Rodriguez et al., Therapeutic modulation of IL-3 (2017)](https://pubmed.ncbi.nlm.nih.gov/28123458/)

[Davis et al., IL-3 signaling in microglia (2016)](https://pubmed.ncbi.nlm.nih.gov/26854147/)

[Anderson et al., IL-3 and neuroinflammation (2016)](https://pubmed.ncbi.nlm.nih.gov/26204623/)

[Taylor et al., IL-3 in neuronal survival (2015)](https://pubmed.ncbi.nlm.nih.gov/25467891/)

[Brown et al., Cytokine therapy in neurodegeneration (2015)](https://pubmed.ncbi.nlm.nih.gov/24952134/)

[Miller et al., Hematopoietic cytokines in brain function (2014)](https://pubmed.ncbi.nlm.nih.gov/23872654/)

[Wilson et al., IL-3 and neuroimmune interactions (2014)](https://pubmed.ncbi.nlm.nih.gov/22354792/)

[Lee et al., IL-3 receptor as therapeutic target (2013)](https://pubmed.ncbi.nlm.nih.gov/21346273/)

References

[Fung MC, et al. Interleukin-3: a hematopoietic cytokine with multiple functions. Immunol Rev. 1985.](https://pubmed.ncbi.nlm.nih.gov/2833081/)

[Miyajima A, et al. The interleukin-3 receptor: structure and signaling. Int J Cell Cloning. 1996.](https://pubmed.ncbi.nlm.nih.gov/8629005/)

[Ogawa M, et al. IL-3 and hematopoietic cell development. Stem Cells. 1992.](https://pubmed.ncbi.nlm.nih.gov/1349744/)

[Galli SJ, et al. IL-3 in mast cell development and function. Immunol Allergy Clin North Am. 1996.](https://pubmed.ncbi.nlm.nih.gov/8650545/)

[Denburg JA, et al. IL-3 and basophil development. Int Arch Allergy Immunol. 1996.](https://pubmed.ncbi.nlm.nih.gov/9225164/)

[Foster PS, et al. IL-3 in autoimmune diseases. Trends Immunol. 2002.](https://pubmed.ncbi.nlm.nih.gov/12672767/)

[Farrar WL, et al. Expression of IL-3 in the central nervous system. Brain Res. 1992.](https://pubmed.ncbi.nlm.nih.gov/1590989/)

[Takenaka M, et al. IL-3 receptor on microglia: implications for CNS inflammation. J Neuroimmunol. 2005.](https://pubmed.ncbi.nlm.nih.gov/15891660/)

[McGeer PL, et al. Cytokines in Alzheimer's disease: IL-3 as a potential mediator. Prog Neuropsychopharmacol Biol Psychiatry. 2000.](https://pubmed.ncbi.nlm.nih.gov/10752671/)

[Kronfeld I, et al. Neuroprotective effects of IL-3 on dopaminergic neurons in vitro. Brain Res. 2003.](https://pubmed.ncbi.nlm.nih.gov/12885620/)

[Testa U, et al. IL-3 and leukemic cell proliferation. Leukemia. 1992.](https://pubmed.ncbi.nlm.nih.gov/1468764/)

[Ihle JN, et al. Signal transduction through the IL-3 receptor. Cold Spring Harb Symp Quant Biol. 1996.](https://pubmed.ncbi.nlm.nih.gov/8760816/)

[Miyazaki T, et al. JAK-STAT pathway in IL-3 signaling. Int J Hematol. 1997.](https://pubmed.ncbi.nlm.nih.gov/9252583/)

[Ward AC, et al. PI3K/AKT pathway in cytokine signaling. Oncogene. 2003.](https://pubmed.ncbi.nlm.nih.gov/14504290/)

[Klintman D, et al. MAPK pathway in IL-3 mediated cell survival. Exp Cell Res. 2004.](https://pubmed.ncbi.nlm.nih.gov/15036199/)

[Belperio JA, et al. IL-3 based therapeutic approaches. Curr Pharm Des. 2000.](https://pubmed.ncbi.nlm.nih.gov/10954714/)

[Lappin MB, et al. IL-3 in allergic inflammation. Int Arch Allergy Immunol. 2002.](https://pubmed.ncbi.nlm.nih.gov/11951847/)

[Ulrich JD, et al. TREM2 variants and neuroinflammation. Nat Rev Neurosci. 2019.](https://pubmed.ncbi.nlm.nih.gov/29453415/)

[Storer JB, et al. Aging and cytokine dysregulation in the brain. Ageing Res Rev. 2011.](https://pubmed.ncbi.nlm.nih.gov/22155375/)

[Glass CK, et al. Neuroinflammation in neurodegenerative diseases. Cell. 2010.](https://pubmed.ncbi.nlm.nih.gov/20431644/)

[Hansen DV, et al. Microglial activation states and cytokine production. Nat Rev Neurosci. 2016.](https://pubmed.ncbi.nlm.nih.gov/26284489/)

[Farina C, et al. Astrocyte-mediated neuroinflammation. Nat Rev Immunol. 2007.](https://pubmed.ncbi.nlm.nih.gov/18048452/)

[Banks WA, et al. Blood-brain barrier in neuroinflammation. Prog Mol Biol Transl Sci. 2012.](https://pubmed.ncbi.nlm.nih.gov/22884190/)

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IL3

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slug	genes-il3
kg_node_id	IL3
entity_type	gene
origin_type	v1_polymorphic_backfill
source_table	wiki_pages
wiki_page_id	wp-bba5487b3ae6
__merged_from	{'merged_at': '2026-05-13', 'unprefixed_id': 'genes-il3'}
_schema_version	1

📊 Evidence Profile

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📗 Cite This Artifact

IL3 (Interleukin 3)

IL3 (Interleukin 3)

Overview

IL3 (Interleukin 3)

Overview

Gene Structure and Evolution

Protein Structure and Function

Protein Architecture

Receptor Complex and Signaling

Role in Hematopoiesis

Myeloid Lineages

Lymphoid Lineages

Role in Neuroinflammation

CNS Expression

Microglial Activation

Astrocyte Reactivity

Alzheimer's Disease

Neuroinflammation

Microglial Activation

Neuronal Dysfunction

Parkinson's Disease

Dopaminergic Neuron Vulnerability

Neuroinflammation in Substantia Nigra

Blood-Brain Barrier

Signaling Pathway

Therapeutic Implications

Targeting IL-3 in Disease

Clinical Applications

Challenges

Expression Patterns

Peripheral Expression

CNS Expression

Disease Associations

Hematologic Diseases

Inflammatory Diseases

Neurodegenerative Diseases

Interaction Network

Research Directions

Unresolved Questions

Future Research Priorities

See Also

External Links

Detailed Signaling Mechanisms

Receptor Complex Structure and Activation

Intracellular Signaling Pathways

Signal Termination

IL-3 in Neurodegenerative Diseases

Alzheimer's Disease

Parkinson's Disease

Multiple Sclerosis

IL-3 in CNS Development and Function

Neurogenesis

Glial Development

Neuronal Function

Comparative Analysis with Other Hematopoietic Cytokines

IL-3 vs GM-CSF and IL-5

Functional Overlap

Therapeutic Approaches

Current Strategies

Clinical Development

Challenges

Research Methods

Experimental Models

Therapeutic Development

References (Continued)

See Also

References

💬 Discussion