EBI3: Epstein-Barr Virus Induced 3 – IL-27 Subunit and Immune Regulator

Comprehensive genomic and functional analysis of EBI3, a key cytokine subunit in IL-27 and IL-35, with roles in immune regulation, inflammation, and cancer.

Gene Information Card

Symbol EBI3
Full Name Epstein-Barr virus induced 3
Gene Type protein-coding
Chromosomal Location 19p13.3
NCBI Gene ID 10148 ncbi.nlm.nih.gov/gene/10148
Ensembl ID ENSG00000105246
UniProt ID Q14213
OMIM ID 605816
HGNC ID 3249
Aliases IL-27B, IL35B, IL27B

Description

EBI3 (Epstein-Barr virus induced 3) encodes a secreted glycoprotein that belongs to the hematopoietin receptor family. It is a subunit of the heterodimeric cytokines interleukin-27 (IL-27) and interleukin-35 (IL-35), where it pairs with p28 (IL-27A) or p35 (IL-12A), respectively. EBI3 is expressed in various immune cells and plays critical roles in regulating T-cell differentiation, inflammation, and immune tolerance. Dysregulation of EBI3 is implicated in autoimmune diseases, infectious diseases, and cancers.

Disease Associations

Disease category Pathophysiological mechanism Genomic evidence
Inflammatory bowel disease EBI3 contributes to IL-35-mediated regulatory T-cell function; altered expression linked to intestinal inflammation PMID: 21706003
Rheumatoid arthritis EBI3 expression in synovial tissue promotes IL-35-mediated suppression of inflammation PMID: 25605269
Multiple sclerosis EBI3 variants associated with risk; IL-35 modulates Th17 responses PMID: 23396211
Gastric cancer EBI3 overexpression correlates with tumor progression and immune evasion via IL-35 signaling PMID: 27864367
Epstein-Barr virus infection EBI3 is induced by EBV and may modulate host immune response PMID: 8642405

Expression Profile

Tissue Expression
Tissue nTPM level
Lymph node 12.5 Medium
Spleen 10.8 Medium
Bone marrow 8.3 Medium
Lung 4.2 Low
Colon 3.1 Low
Small intestine 2.9 Low
Cell Line Expression
Cell Line nTPM Notes
THP-1 (monocyte) 15.2 High expression after LPS stimulation
Jurkat (T-cell) 8.7 Constitutive expression
Raji (B-cell) 6.4 EBV-positive line shows elevated expression
HEK293 1.2 Low baseline expression
Data source:Human Protein Atlas(proteinatlas.org)

Mutations & Variants

Hotspot Mutations
Variant Type Frequency Functional Description
c.1A>G (p.Met1?) missense <0.01% Potential loss of start codon; functional impact unknown
c.304C>T (p.Arg102Trp) missense <0.01% Located in fibronectin type III domain; may affect protein stability
c.487G>A (p.Gly163Ser) missense <0.01% Rare variant; no known disease association
Mutation functional classification

Loss of Function (LOF)

No confirmed loss-of-function mutations reported in EBI3; predicted start-loss variant may reduce translation.

Gain of Function (GOF)

No gain-of-function mutations described in the literature.

Dominant Negative (DN)

No dominant-negative mutations reported for EBI3.

Pathways

IL-27 signaling pathway (Reactome: R-HSA-9020958)
IL-35 signaling pathway (Reactome: R-HSA-9020959)
Cytokine-cytokine receptor interaction (KEGG: hsa04060)
JAK-STAT signaling pathway (KEGG: hsa04630)

Protein Summary

EBI3 is a 34 kDa secreted glycoprotein that forms heterodimers with IL-27A (p28) to create IL-27, or with IL-12A (p35) to create IL-35. It contains a fibronectin type III domain and a WSXWS motif characteristic of class I cytokine receptors. EBI3 is primarily expressed in antigen-presenting cells, B cells, and T cells. IL-27 promotes Th1 differentiation and suppresses Th17 responses, while IL-35 is an immunosuppressive cytokine produced by regulatory T cells. EBI3 has been implicated in autoimmune diseases, chronic inflammation, and tumor immune evasion.

Related Products

Product name Cat.No. Species Gene ID
EBI3 Knockout HEK293 Cell Line EDJ-KQ2551 Human 10148 Details Get a Quote
EBI3 Knockout A-549 Cell Line EDJ-KQ24583 Human 10148 Details Get a Quote
EBI3 Knockout HeLa Cell Line EDJ-KQ55328 Human 10148 Details Get a Quote
EBI3 Knockout HCT 116 Cell Line EDJ-KQ72270 Human 10148 Details Get a Quote
Displaying Records 1 To 4 Of 4 Records
Contact Us
*
*
*
*
How did you hear about us: