Seroatlas · Human Serome Atlas

CXCR3

C-X-C chemokine receptor type 3

Also known as: CD183, CKR-L2, CMKAR3, CXCR3_HUMAN, GPR9, IP10-R, MigR

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
P49682
Gene
CXCR3
Ensembl
ENSG00000186810
Chromosome
X
Canonical length
368 aa
Protein class
CD markers, G-protein coupled receptors, Predicted membrane proteins

OverviewNCBI Gene

This gene encodes a G protein-coupled receptor with selectivity for three chemokines, termed CXCL9/Mig (monokine induced by interferon-g), CXCL10/IP10 (interferon-g-inducible 10 kDa protein) and CXCL11/I-TAC (interferon-inducible T cell a-chemoattractant). Binding of chemokines to this protein induces cellular responses that are involved in leukocyte traffic, most notably integrin activation, cytoskeletal changes and chemotactic migration. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. One of the isoforms (CXCR3-B) shows high affinity binding to chemokine, CXCL4/PF4 (PMID:12782716). [provided by RefSeq, Jun 2011]

Canonical amino-acid sequenceUniProt

368 residues, UniProt reviewed canonical sequence.

>P49682|CXCR3
     1  MVLEVSDHQV LNDAEVAALL ENFSSSYDYG ENESDSCCTS PPCPQDFSLN FDRAFLPALY
    61  SLLFLLGLLG NGAVAAVLLS RRTALSSTDT FLLHLAVADT LLVLTLPLWA VDAAVQWVFG
   121  SGLCKVAGAL FNINFYAGAL LLACISFDRY LNIVHATQLY RRGPPARVTL TCLAVWGLCL
   181  LFALPDFIFL SAHHDERLNA THCQYNFPQV GRTALRVLQL VAGFLLPLLV MAYCYAHILA
   241  VLLVSRGQRR LRAMRLVVVV VVAFALCWTP YHLVVLVDIL MDLGALARNC GRESRVDVAK
   301  SVTSGLGYMH CCLNPLLYAF VGVKFRERMW MLLLRLGCPN QRGLQRQPSS SRRDSSWSET
   361  SEASYSGL

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against CXCR3 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
Cell surface
Secreted
No
Transmembrane segments
7
Mean surface accessibility (rSASA)
0.36
Highest tissue expression
15 nTPM

Expression across tissuesHPA

Tissue

  • lymph node: 15 nTPM
  • spleen: 7.1 nTPM
  • bone marrow: 6.8 nTPM
  • small intestine: 6 nTPM
  • appendix: 5.5 nTPM
  • duodenum: 5.1 nTPM

Single-cell type

  • pdcs: 110 nCPM
  • t-cells: 40 nCPM
  • enterocytes: 15 nCPM
  • plasma cells: 14 nCPM
  • nk-cells: 11 nCPM
  • b-cells: 6.9 nCPM

Immune cell

  • plasmacytoid DC: 307 nTPM
  • NK-cell: 200 nTPM
  • memory CD8 T-cell: 125 nTPM
  • memory CD4 T-cell: 91 nTPM
  • T-reg: 90 nTPM
  • gdT-cell: 81 nTPM

Brain region

  • cerebral cortex: 1.5 nTPM
  • medulla oblongata: 1.2 nTPM
  • cerebellum: 1.1 nTPM
  • hippocampal formation: 1.1 nTPM
  • amygdala: 1 nTPM
  • thalamus: 1 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about CXCR3.

Disease | ImmuneIEDB

Conditions an epitope on CXCR3 was assayed in.

ReferencesPubMed · IEDB

Publications for CXCR3 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.

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. IEDB — curated epitope assays from the Immune Epitope Database (Vita et al., Nucleic Acids Research 2019). 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)
0.97
gnomAD pLI
0.18
gnomAD missense Z
1.74
DepMap mean gene effect
0
DepMap dependency class
none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 2% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of CXCR3 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads CXCR3 as an antibody target. Whether an autoantibody or antibody against CXCR3 could matter depends on whether native CXCR3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

CXCR3 is annotated at the cell surface, where native CXCR3 is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.

Annotation status

The present source text does not explicitly label CXCR3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/CXCR3. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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