CD80

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CD80
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl

ENSG00000121594

ENSMUSG00000075122

UniProt

P33681

Q00609

RefSeq (mRNA)

NM_005191

NM_009855
NM_001359898

RefSeq (protein)

NP_005182

NP_033985
NP_001346827

Location (UCSC)Chr 3: 119.52 – 119.56 MbChr 16: 38.28 – 38.32 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

The Cluster of differentiation 80 (also CD80 and B7-1) is a B7, type I membrane protein

CTLA-4 (CD152) and the p75 neurotrophin receptor .[6][7]

Structure

CD80 is a member of the B7 family, which consists of molecules present at APCs and their receptors present on the T-cells.[7] CD80 is present specifically on DC, activated B-cells, and macrophages, but also T-cells[7][8] CD80 is also a transmembrane glycoprotein and a member of the Ig superfamily.[7] It is composed of 288 amino acids, and its mass is 33 kDa.[8] It consists of two Ig-like extracellular domains (208 AA), a transmembrane helical segment (21 AA), and a short cytoplasmic tail (25 AA).[7][8][9] The Ig-like extracellular domains are formed by single V-type and C2-type domains.[7][6][10] It is expressed as both monomers or dimers, but predominantly dimers.[7][10][11] These two forms exist in dynamic equilibrium.[12]

CD80 shares 25% of sequences with

CTLA-4 than CD86. Moreover, CD80 interacts with its ligand with faster binding kinetics and slower dissociation constants than CD86. Both human CD80 and CD86 are located at chromosome 3; the exact region is 3q13.3-q21.[7]

Human and murine CD80 share approximately 44% of sequences. Also both human and murine CD80 are able to cross-react with both human and murine CD28. This indicates that the binding site of CD80 is conserved.[7][12]

Function

CD80 can be found on the surface of various

dendritic cells.[6][7][13] CD80 has a crucial role in modulating T-cell immune function as a checkpoint protein at the immunological synapse.[14]

CD80 is the ligand for the proteins

T-cells.[6][13] Interaction of CD80 with CD28 triggers costimulatory signals and results in enhanced and sustained T-cell activation. In contrast, contrary interaction of CD80 with CTLA-4 inhibits parts of T-cell effector function. These two ligands are structurally homologous, and they compete with each other for binding sites.[14] However, the bond with CTLA-4 has up to 2500 fold higher avidity than with CD28.[7] This illustrates that inhibitory interaction with CTLA-4 is predominant.[14]

CD80 binds to

T-cells that result in T and B-cell activation, proliferation and differentiation.[11]

When stimulated by CD80,

cytotoxic T-cell.[13][16] The expression of CD80, as well as CD86, is increased by the presence of microbes and cytokines, which is the consequence of the presence of microbes. This mechanism ensures that costimulatory molecules for T-cells are present at the right time.[7]

CD80, often in tandem with

macrophages with CD80 via CD28.[22] Last but not least, the interaction of CD80 and CD28 enhances cell‐cycle progression by upregulating the expression levels of D‐cyclin.[14]

In contrast to the stimulatory interaction with

self-antigen.[18]

In addition to interactions with

B-cells may regulate antibody secretion during infection.[25]

Another ligand of CD80 is programmed death-ligand 1 (PD‐L1), expressed on the surface of T-cells, B-cells, DCs, and macrophages. This interaction is inhibiting and causes a reduction in T-cell activation as well as reduction of cytokine production. Its dissociation constant with CD80 is between the CD28 and CTLA-40 (Kd = 1.4 μM).[14][26]

Clinical significance

The complicated role CD80 plays in immune system regulation presents an opportunity for CD80 interactions to go rogue in various diseases. The up-regulation of CD80 has been linked to various

systemic lupus erythematosus[28] and sepsis[29] (which may partly be due to over-active T-cells), and CD80 has also been shown to help spread of HIV infection in the body.[30] CD80 is also linked to various cancers, though some experience CD80 induced tolerance via possible regulatory T-cell interaction.[31] Others experience inhibited growth and metastasis-related to CD80 up-regulation,[32]
further exemplifies the complicated role CD80 plays.

The triggering of

Natural Killer cell-mediated death via CD80 interactions has been explored as possible cancer immunotherapy by inducing CD80 expression on tumor cells.[23]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000121594 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000075122 – Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ McKusick, V. A., & Converse, P. J. (2016, August 05). CD80 Antigen; CD80. Retrieved May 29, 2019
  6. ^
    PMID 7545666
    .
  7. ^
    ISBN 978-0-12-802585-7
    .
  8. ^ a b c "CD80 - T-lymphocyte activation antigen CD80 precursor - Homo sapiens (Human) - CD80 gene & protein". www.uniprot.org. Retrieved 2021-06-09.
  9. OCLC 1173994133
    .
  10. ^
    PMID 16413062
    .
  11. ^
    PMID 16221763
    .
  12. ^
    PMID 10661405
    .
  13. ^ a b c Owen JA, Punt J, Stranford SA, Jones PP, Kuby J (2013). Kuby Immunology (7th ed.). New York: W.H. Freeman and Company.
  14. ^
    S2CID 201748060
    .
  15. PMID 9053440
    .
  16. PMID 15197224
    .
  17. PMID 19707331
    .
  18. ^
    PMID 14978077
    .
  19. PMID 7621080
    .
  20. PMID 11544316
    .
  21. S2CID 6080497
    .
  22. ^
    PMID 19672303
    .
  23. ^
    PMID 8885864
    .
  24. PMID 11160311
    .
  25. PMID 19933871
    .
  26. PMID 17629517
    .
  27. PMID 7500044
    .
  28. PMID 15870153
    .
  29. PMID 17989345
    .
  30. PMID 7534204
    .
  31. PMID 16818658
    .
  32. S2CID 82772085
    .

External links
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