IFNL3
Interferon lambda-3
Also known as: IFNL3_HUMAN, IL-28B, IL28B, IL28C
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q8IZI9
- Gene
- IFNL3
- Ensembl
- ENSG00000197110
- Chromosome
- 19
- Canonical length
- 196 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 28A (IL28A), 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
196 residues, UniProt reviewed canonical sequence.
>Q8IZI9|IFNL3
1 MTGDCMPVLV LMAAVLTVTG AVPVARLRGA LPDARGCHIA QFKSLSPQEL QAFKRAKDAL
61 EESLLLKDCK CRSRLFPRTW DLRQLQVRER PVALEAELAL TLKVLEATAD TDPALGDVLD
121 QPLHTLHHIL SQLRACIQPQ PTAGPRTRGR LHHWLHRLQE APKKESPGCL EASVTFNLFR
181 LLTRDLNCVA SGDLCVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against IFNL3 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)
- 0.37
- Highest tissue expression
- 0.2 nTPM
Expression across tissuesHPA
Tissue
- testis: 0.2 nTPM
- amygdala: 0.1 nTPM
- cerebellum: 0.1 nTPM
- cerebral cortex: 0.1 nTPM
- salivary gland: 0.1 nTPM
- skin: 0.1 nTPM
Single-cell type
- retinal bipolar cells: 0.3 nCPM
- early spermatids: 0.2 nCPM
- brain excitatory neurons: 0.1 nCPM
- late spermatids: 0.1 nCPM
- megakaryocyte progenitors: 0.1 nCPM
- migrating cytotrophoblasts: 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: 0.2 nTPM
- cerebral cortex: 0.1 nTPM
- hippocampal formation: 0.1 nTPM
- hypothalamus: 0.1 nTPM
- white matter: 0.1 nTPM
- basal ganglia: 0 nTPM
ReferencesPubMed · IEDB
Publications for IFNL3 from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.
Reference: AutoantibodyPubMed
3 publications
- Unbiased discovery of autoantibodies associated with severe COVID-19 via genome-scale self-assembled DNA-barcoded protein libraries.
2022 · Nat Biomed Eng · RCR 3.7 · 54 citations - Membrane Proteome-Wide Screening of Autoantibodies in CIDP Using Human Cell Microarray Technology.
2024 · Neurol Neuroimmunol Neuroinflamm · RCR 1.7 · 8 citations - Neutralizing IFNL3 Autoantibodies in Severe COVID-19 Identified Using Molecular Indexing of Proteins by Self-Assembly.
2021 · bioRxiv · RCR 0.3 · 6 citations
Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.
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)
- 1.91
- gnomAD pLI
- 0
- gnomAD missense Z
- -1.16
- DepMap mean gene effect
- -0.07
- 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
- negative regulation of viral genome replication
- 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 IFNL3 as an antibody target. Whether an autoantibody or antibody against IFNL3 could matter depends on whether native IFNL3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
IFNL3 is annotated as secreted, so native IFNL3 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 IFNL3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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