IFNL2
Interferon lambda-2
Also known as: IFNL2_HUMAN, IL-28A, IL28A
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q8IZJ0
- Gene
- IFNL2
- Ensembl
- ENSG00000183709
- Chromosome
- 19
- Canonical length
- 200 aa
- Protein class
- Predicted secreted proteins
- Secretome location
- Secreted to blood
OverviewNCBI Gene
This gene encodes a cytokine distantly related to type I interferons and the IL-10 family. This gene, interleukin 28B (IL28B), and interleukin 29 (IL29) are three closely related cytokine genes that form a cytokine gene cluster on a chromosomal region mapped to 19q13. Expression of the cytokines encoded by the three genes can be induced by viral infection. All three cytokines have been shown to interact with a heterodimeric class II cytokine receptor that consists of interleukin 10 receptor, beta (IL10RB) and interleukin 28 receptor, alpha (IL28RA). [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
200 residues, UniProt reviewed canonical sequence.
>Q8IZJ0|IFNL2
1 MKLDMTGDCT PVLVLMAAVL TVTGAVPVAR LHGALPDARG CHIAQFKSLS PQELQAFKRA
61 KDALEESLLL KDCRCHSRLF PRTWDLRQLQ VRERPMALEA ELALTLKVLE ATADTDPALV
121 DVLDQPLHTL HHILSQFRAC IQPQPTAGPR TRGRLHHWLY RLQEAPKKES PGCLEASVTF
181 NLFRLLTRDL NCVASGDLCVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against IFNL2 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Secreted
- Secreted
- Yes
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.38
- Highest tissue expression
- 0.4 nTPM
Expression across tissuesHPA
Tissue
- pancreas: 0.4 nTPM
- testis: 0.2 nTPM
- skin: 0.1 nTPM
- adipose tissue: 0 nTPM
- adrenal gland: 0 nTPM
- amygdala: 0 nTPM
Single-cell type
- epicardial cells: 2.3 nCPM
- granulosa cells: 0.8 nCPM
- cdc: 0.1 nCPM
- early primary spermatocytes: 0.1 nCPM
- epididymal principal cells: 0.1 nCPM
- pancreatic acinar cells: 0.1 nCPM
Immune cell
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- eosinophil: 0 nTPM
- gdT-cell: 0 nTPM
- intermediate monocyte: 0 nTPM
- MAIT T-cell: 0 nTPM
Brain region
- amygdala: 0.3 nTPM
- cerebellum: 0.3 nTPM
- cerebral cortex: 0.3 nTPM
- hippocampal formation: 0.3 nTPM
- basal ganglia: 0.2 nTPM
- hypothalamus: 0.1 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.87
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.24
- DepMap mean gene effect
- 0.09
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cell surface receptor signaling pathway via JAK-STAT
- cellular response to virus
- defense response to virus
- innate immune response
- mucosal immune response
- positive regulation of immune response
- type III interferon-mediated signaling pathway
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads IFNL2 as an antibody target. Whether an autoantibody or antibody against IFNL2 could matter depends on whether native IFNL2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
IFNL2 is annotated as secreted, so native IFNL2 circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.
Annotation status
The present source text does not explicitly label IFNL2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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