CD86
T-lymphocyte activation antigen CD86
Also known as: B7-2, B7.2, CD28LG2, CD86_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P42081
- Gene
- CD86
- Ensembl
- ENSG00000114013
- Chromosome
- 3
- Canonical length
- 329 aa
- Protein class
- CD markers, FDA approved drug targets, Predicted intracellular proteins, Predicted membrane proteins
- Subcellular location
- Plasma membrane,Centriolar satellite
- Quaternary structure
- Homodimer
OverviewNCBI Gene
This gene encodes a type I membrane protein that is a member of the immunoglobulin superfamily. This protein is expressed by antigen-presenting cells, and it is the ligand for two proteins at the cell surface of T cells, CD28 antigen and cytotoxic T-lymphocyte-associated protein 4. Binding of this protein with CD28 antigen is a costimulatory signal for activation of the T-cell. Binding of this protein with cytotoxic T-lymphocyte-associated protein 4 negatively regulates T-cell activation and diminishes the immune response. Alternative splicing results in several transcript variants encoding different isoforms.[provided by RefSeq, May 2011]
Canonical amino-acid sequenceUniProt
329 residues, UniProt reviewed canonical sequence.
>P42081|CD86
1 MDPQCTMGLS NILFVMAFLL SGAAPLKIQA YFNETADLPC QFANSQNQSL SELVVFWQDQ
61 ENLVLNEVYL GKEKFDSVHS KYMGRTSFDS DSWTLRLHNL QIKDKGLYQC IIHHKKPTGM
121 IRIHQMNSEL SVLANFSQPE IVPISNITEN VYINLTCSSI HGYPEPKKMS VLLRTKNSTI
181 EYDGVMQKSQ DNVTELYDVS ISLSVSFPDV TSNMTIFCIL ETDKTRLLSS PFSIELEDPQ
241 PPPDHIPWIT AVLPTVIICV MVFCLILWKW KKKKRPRNSY KCGTNTMERE ESEQTKKREK
301 IHIPERSDEA QRVFKSSKTS SCDKSDTCFLocalizationUniProt · AlphaFold · HPA
Whether an antibody against CD86 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
- 1
- Mean surface accessibility (rSASA)
- 0.42
- Highest tissue expression
- 33 nTPM
Expression across tissuesHPA
Tissue
- appendix: 33 nTPM
- lymph node: 27 nTPM
- spleen: 22 nTPM
- tonsil: 21 nTPM
- lung: 18 nTPM
- placenta: 14 nTPM
Single-cell type
- cdc: 462 nCPM
- microglia: 366 nCPM
- macrophages: 338 nCPM
- monocytes: 297 nCPM
- hofbauer cells: 273 nCPM
- kupffer cells: 260 nCPM
Immune cell
- non-classical monocyte: 86 nTPM
- classical monocyte: 80 nTPM
- intermediate monocyte: 79 nTPM
- myeloid DC: 79 nTPM
- memory B-cell: 41 nTPM
- total PBMC: 34 nTPM
Brain region
- white matter: 19 nTPM
- medulla oblongata: 12 nTPM
- hypothalamus: 10 nTPM
- pons: 9.2 nTPM
- spinal cord: 8.3 nTPM
- thalamus: 8.1 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about CD86.
Disease | AutoantibodyPubMed
Conditions in which antibodies against CD86 are reported. Each links to that disease's full target list.
ReferencesPubMed · IEDB
Publications for CD86 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
12 publications
- Preferential dependence of autoantibody production in murine lupus on CD86 costimulatory molecule.
1995 · Eur J Immunol · RCR 2.6 · 131 citations - Autoantibodies to T cell costimulatory molecules in systemic autoimmune diseases.
1999 · J Immunol · RCR 1.5 · 63 citations - Opposing effects of anti-activation-inducible lymphocyte-immunomodulatory molecule/inducible costimulator antibody on the development of acute versus chronic graft-versus-host disease.
2001 · J Immunol · RCR 0.9 · 52 citations - B7 costimulation in the development of lupus: autoimmunity arises either in the absence of B7.1/B7.2 or in the presence of anti-b7.1/B7.2 blocking antibodies.
1999 · J Immunol · RCR 0.7 · 41 citations - Treatment with anti-CD86 costimulatory molecule prevents the autoimmune lesions in murine Sjögren's syndrome (SS) through up-regulated Th2 response.
2000 · Clin Exp Immunol · RCR 0.7 · 38 citations
Show 7 more
- Abatacept downregulates Fcγ receptor I on circulating monocytes: a potential therapeutic mechanism in patients with rheumatoid arthritis.
2022 · Arthritis Res Ther · RCR 0.6 · 8 citations - B7-1 and B7-2 co-stimulatory molecules are required for mercury-induced autoimmunity.
2002 · Clin Exp Immunol · RCR 0.4 · 20 citations - Direct suppression of autoaggressive CD8+ T cells with CD80/86 blockade in CD8+ T cell-mediated polymyositis models of mice.
2017 · Clin Exp Rheumatol · RCR 0.3 · 9 citations - A monoclonal antibody against CD86 and its protection in a murine lupus nephritis model of chronic graft-versus-host disease.
2017 · Immunopharmacol Immunotoxicol · RCR 0.3 · 7 citations - Effects of anti-B7 monoclonal antibodies on humoral immune responses.
1999 · J Autoimmun · RCR 0.3 · 12 citations - B7-1 costimulatory molecule is critical for the development of experimental autoimmune myasthenia gravis.
2003 · J Immunol · RCR 0.2 · 12 citations - The Th2-response in mercuric chloride-induced autoimmunity requires continuing costimulation via CD28.
2002 · Clin Exp Immunol · RCR 0.1 · 7 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)
- 0.35
- gnomAD pLI
- 0.95
- gnomAD missense Z
- 1.08
- DepMap mean gene effect
- -0.02
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- adaptive immune response
- B cell activation
- cell surface receptor signaling pathway
- cellular response to lipopolysaccharide
- immune response
- negative regulation of T cell activation
- negative regulation of T cell proliferation
- negative regulation of T cell receptor signaling pathway
- positive regulation of cell population proliferation
- positive regulation of DNA-templated transcription
- positive regulation of immunoglobulin production
- positive regulation of interleukin-2 production
- positive regulation of interleukin-4 production
- positive regulation of lymphotoxin A production
- positive regulation of non-canonical NF-kappaB signal transduction
- positive regulation of T cell proliferation
- positive regulation of T cell receptor signaling pathway
- positive regulation of T-helper 2 cell differentiation
- T cell activation
- T cell costimulation
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of CD86 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 CD86 as an antibody target. Whether an autoantibody or antibody against CD86 could matter depends on whether native CD86 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CD86 is annotated at the cell surface, where native CD86 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 CD86 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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