Affinage

CD86

T-lymphocyte activation antigen CD86 · UniProt P42081

Length
329 aa
Mass
37.7 kDa
Annotated
2026-04-28
100 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD86 (B7-2) is a monomeric costimulatory ligand expressed on antigen-presenting cells that engages CD28 and CTLA-4 on T cells to regulate adaptive immune activation, peripheral tolerance, and bidirectional signaling in both APCs and B cells. Engagement of CD28 by CD86 activates PI3-kinase-dependent IL-2 production and Rac1-driven actin cytoskeleton rearrangement at the T cell–APC contact site, while the CD86 V domain alone is sufficient for CTLA-4 binding, which triggers pH-dependent CTLA-4 recycling and iterative transendocytosis distinct from the CD80–CTLA-4 fate (PMID:7584133, PMID:9551951, PMID:35999394, PMID:8609386). CD86 surface levels are controlled post-translationally by MARCH1-mediated ubiquitination at K267 sustained by autocrine IL-10, and transcriptionally by Tet2/Tet3-dependent epigenetic silencing via HDAC1/2 recruitment at the Cd86 locus (PMID:21849678, PMID:32572241). CD86 also mediates reverse signaling: in B cells, its cytoplasmic domain cooperates with prohibitin adaptors to activate NF-κB and promote IgG1 class-switched antibody secretion, and in dendritic cells it signals through p38 MAPK to induce IL-6; additionally, CD86 serves as a cellular receptor for species B adenoviruses and lymphotropic HCV (PMID:23241883, PMID:19933871, PMID:15467723, PMID:16920215, PMID:28067225).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1995 High

    Establishing that CD86-mediated T cell costimulation requires PI3-kinase signaling through CD28 resolved which downstream pathway is essential for IL-2 production upon CD86 engagement.

    Evidence CD28 cytoplasmic domain point mutants (Y191F, M194C) co-stimulated with CD86-expressing CHO cells, IL-2 readout

    PMID:7584133

    Open questions at the time
    • Whether PI3K is the sole pathway or acts in concert with other kinases downstream of CD86–CD28
    • No direct structural mapping of CD28–PI3K interaction in the context of CD86 engagement
  2. 1996 Medium

    Demonstrating that the CD86 V domain alone suffices for CTLA-4 binding — unlike CD80, which requires both domains — established a fundamental structural distinction between the two B7 ligands in receptor engagement.

    Evidence Domain-swapped and truncated CD80/CD86 chimeras tested for CTLA-4 binding

    PMID:8609386

    Open questions at the time
    • Atomic-resolution basis for V-domain sufficiency not yet defined at this point
    • Whether V-domain sufficiency translates to differential signaling outcomes through CTLA-4
  3. 1998 High

    Two advances defined CD86's roles in cytoskeletal signaling and peripheral tolerance: CD86–CD28 engagement selectively translocates Rac1 (not Rho) to the T cell–APC contact and remodels actin, while constitutive B7-2 expression on anergic B cells prevents Fas-mediated deletion, revealing that CD86 repression is required for peripheral B cell tolerance.

    Evidence Confocal imaging of Rac1/talin translocation upon CD86–CD28 ligation; B7-2 transgenic mice with in vivo B cell fate tracking

    PMID:9551951 PMID:9705947

    Open questions at the time
    • The GEF linking CD28 engagement to Rac1 activation is unidentified
    • Whether CD86 repression on anergic B cells is transcriptional or post-translational was unknown
  4. 1999 High

    Comparative biochemical analysis showed that CD86 and CD80 trigger qualitatively different proximal signals through CD28 — CD86 ligation does not induce detectable CD28 tyrosine phosphorylation or robust PI3K recruitment, yet both ligands converge on shared distal events including CBL/VAV phosphorylation and NFAT activation.

    Evidence CHO transfectants expressing CD80 or CD86, immunoprecipitation and Western blot for CD28 phosphorylation, PI3K association, downstream transcription factor activation

    PMID:9915850

    Open questions at the time
    • How CD86 achieves IL-2 production despite weak CD28 tyrosine phosphorylation
    • Whether quantitative rather than qualitative differences in PI3K recruitment account for these results
  5. 2001 High

    The crystal structure of CTLA-4/CD86 revealed that dimerization interfaces of both proteins position binding sites to favor formation of an alternating periodic lattice, providing a structural model for immunological synapse organization.

    Evidence X-ray crystallography at 3.2-Å resolution

    PMID:11279501

    Open questions at the time
    • Whether the lattice model occurs in physiological cell–cell contacts
    • No dynamics or stoichiometry information at cell surfaces
  6. 2004 High

    Two studies established CD86 as a bidirectional signaling molecule: reverse signaling through CD86 on DCs induces IL-6 via p38 MAPK to counteract immunosuppressive tryptophan catabolism, while IL-4-driven CD86 upregulation on monocytes requires JAK/STAT6 and MEK/ERK1/2 and is negatively regulated by PKCδ.

    Evidence Soluble CD28 treatment of DCs with p38 inhibition and in vivo validation; pharmacological kinase inhibitor dissection in monocytes

    PMID:14636897 PMID:15467723

    Open questions at the time
    • The proximal receptor complex mediating reverse signaling in DCs is undefined
    • Whether PKCδ directly phosphorylates CD86 or acts indirectly
  7. 2005 Medium

    FRET-based measurements confirmed CD86 exists as a monomer on the cell surface, contrasting with CD80 homodimers, and excluded CD80–CD86 hetero-oligomers — clarifying the oligomeric state relevant to receptor engagement.

    Evidence Photobleaching FRET on live cells expressing CD80 and/or CD86

    PMID:16413062

    Open questions at the time
    • Whether ligand engagement or clustering at the synapse induces transient dimerization
    • Monomer status established on transfected cells, not primary APCs
  8. 2006 High

    Identification of CD86 as a cellular attachment receptor for species B adenoviruses expanded CD86's function beyond immune costimulation to pathogen entry.

    Evidence Competitive infection blocking with fiber-knob domain, CD86-expressing CHO cells, multi-serotype infection assays

    PMID:16920215

    Open questions at the time
    • Whether CD86 mediates virus internalization or only attachment
    • Structural basis of fiber-knob–CD86 interaction unknown
  9. 2008 High

    HIV-1 Nef was shown to remove CD86 from the APC surface via a clathrin/dynamin-independent, actin-dependent pathway and reroute it to the Golgi through de novo Rab11 recruitment, revealing a viral immune evasion mechanism targeting CD86 trafficking.

    Evidence Fluorescence microscopy, dominant-negative Rab constructs, endosomal marker colocalization in Nef-expressing cells

    PMID:18764822

    Open questions at the time
    • Whether Nef directly binds CD86 or acts through an intermediate adaptor
    • Functional consequence for T cell activation not directly measured
  10. 2009 High

    Demonstrating that CD86 reverse signaling in B cells promotes IgG secretion and XBP-1 splicing in class-switched B cells established a cell-intrinsic role for CD86 beyond costimulation.

    Evidence Mixed bone marrow chimeras with B cell-specific B7-1/2 deficiency, in vitro CD86 engagement, XBP-1 splicing and IgG ELISA

    PMID:19933871

    Open questions at the time
    • Identity of the natural ligand triggering reverse signaling in vivo
    • Whether XBP-1 induction is direct or secondary to increased secretory load
  11. 2011 High

    Two studies defined post-translational and transcriptional control of CD86: MARCH1 ubiquitinates CD86 at K267 to limit surface expression under autocrine IL-10 control in DCs, while Toxoplasma gondii induces CD86 transcription via JNK (not ERK/p38) independently of TLR/MyD88/TRIF.

    Evidence MARCH1 KO mice and K267R mutant CD86 with T cell activation assays; MAPK inhibitors and MyD88/TRIF KO macrophages with B7-2 blocking antibodies

    PMID:21849678 PMID:21911468

    Open questions at the time
    • Whether MARCH1 ubiquitination triggers lysosomal degradation or recycling of CD86
    • Identity of the parasite-derived signal activating JNK for CD86 induction
  12. 2012 High

    Prohibitin 1/2 were identified as transmembrane adaptors that bind the CD86 cytoplasmic domain and mediate NF-κB activation and IgG1 production in B cells, defining the first signaling intermediates in CD86 reverse signaling; separately, iTregs were shown to acquire CD86 from DCs via trogocytosis in a CTLA-4/CD28-independent manner, gaining enhanced suppressive capacity.

    Evidence Proteomic identification and Co-IP of Phb1/2 with CD86, shRNA knockdown, cytoplasmic domain mutants; co-incubation of CD80/86 double-KO iTregs with mature DCs

    PMID:22307040 PMID:23241883

    Open questions at the time
    • Whether Phb1/2 form a stable complex with CD86 or are recruited transiently
    • Mechanism by which acquired CD86 enhances Treg suppression is unclear
  13. 2016 High

    Bacterial superantigens were found to bridge CD86 and CD28 homodimer interfaces simultaneously via the same 12-aa structural motif, explaining superantigen-driven cytokine hyperproduction and providing a pharmacological target — CD86 dimer-interface mimetic peptides block this pathological interaction.

    Evidence Binding assays mapping the superantigen–CD86/CD28 interface, mimetic peptide competition, in vivo superantigen lethality rescue

    PMID:27708164

    Open questions at the time
    • Whether all superantigen families share this bridging mechanism
    • Structural co-crystal of superantigen with both CD86 and CD28 is lacking
  14. 2017 Medium

    CD86 was identified as a co-receptor for lymphotropic HCV infection of B cells, and CD86-dependent HCV infection was shown to impair memory B cell recall responses, linking CD86's receptor function to viral immunopathology; separately, CD86 intrinsic signaling via its cytosolic domain was found to promote myeloma cell survival through IRF4 maintenance.

    Evidence cDNA library screen for HCV co-receptor, CD86 silencing blocks infection, antigen recall assays; CD86 silencing and cytosolic domain deletion in myeloma cells with IRF4/integrin readouts

    PMID:28067225 PMID:29296880

    Open questions at the time
    • Whether CD86 directly binds HCV envelope glycoproteins or acts indirectly
    • Whether CD86-dependent myeloma survival operates in primary patient samples
    • HCV co-receptor function awaits independent replication
  15. 2020 High

    Tet2/Tet3 were shown to be required for epigenetic silencing of CD86 on chronically antigen-exposed B cells by recruiting HDAC1/2 to the Cd86 locus, establishing an epigenetic layer of CD86 regulation essential for self-tolerance.

    Evidence B cell-specific Tet2/Tet3 double-KO mice, ChIP for HDAC1/2 at Cd86, anti-CD86 blockade partially rescuing aberrant activation

    PMID:32572241

    Open questions at the time
    • Whether Tet2/3 act through 5hmC-dependent or -independent mechanisms at Cd86
    • Which specific CpGs at the Cd86 locus are functionally relevant
  16. 2022 High

    Revealing that CTLA-4 undergoes pH-dependent detachment from CD86 and recycles for iterative transendocytosis — unlike its irreversible lysosomal fate with CD80 — resolved the long-standing question of why CTLA-4 is a more efficient checkpoint for CD86 than CD80, and showed that autoimmune disease mutations selectively disrupt CD86 transendocytosis.

    Evidence Live-cell imaging, pH-shift assays, biochemical fractionation, disease-associated CTLA-4 mutation analysis

    PMID:35999394

    Open questions at the time
    • Structural basis for pH-dependent CTLA-4/CD86 dissociation at atomic resolution
    • Whether iterative transendocytosis quantitatively accounts for CD86 regulation in vivo

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the GEF linking CD28–CD86 engagement to Rac1 activation, the structural basis for pH-dependent CTLA-4/CD86 dissociation, the natural in vivo ligand triggering CD86 reverse signaling in B cells, and whether CD86's viral receptor functions for HCV and adenovirus involve direct envelope/capsid binding or accessory factors.
  • No structural model of CD86 reverse signaling complex with prohibitins
  • Quantitative contribution of MARCH1 vs. Tet2/3 epigenetic regulation to steady-state CD86 levels in vivo not determined
  • No reconstituted system demonstrating iterative transendocytosis cycle kinetics

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 5 GO:0060089 molecular transducer activity 4 GO:0001618 virus receptor activity 2
Localization
GO:0005886 plasma membrane 4 GO:0031410 cytoplasmic vesicle 2 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-168256 Immune System 10 R-HSA-162582 Signal Transduction 6 R-HSA-1643685 Disease 4
Partners
CD28CTLA4MARCH1PHBPHB2RAB11A

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Crystal structure of the human CTLA-4/B7-2 (CD86) complex at 3.2-Å resolution revealed that the unusual dimerization properties of both CTLA-4 and B7-2 place their ligand-binding sites distal to the dimer interface, promoting formation of an alternating CTLA-4/B7-2 network that provides a model for periodic organization within the immunological synapse. X-ray crystallography (3.2-Å resolution crystal structure) Nature High 11279501
2022 CTLA-4 targets both CD80 and CD86 for destruction via transendocytosis, but with distinct fates: in the presence of CD86, CTLA-4 detaches in a pH-dependent manner and recycles back to the cell surface for further transendocytosis, whereas in the presence of CD80, CTLA-4 remains ligand-bound and is ubiquitylated and trafficked to lysosomes. Clinically relevant autoimmune disease mutations selectively disrupted CD86 transendocytosis by affecting either CTLA-4 recycling or CD86 binding. Live-cell imaging, biochemical fractionation, mutagenesis, pH-shift assays, analysis of disease-associated mutations Nature immunology High 35999394
2011 CD86 is ubiquitinated by the MARCH1 E3 ubiquitin ligase at lysine 267 in dendritic cells, and this ubiquitination is a key mechanism controlling CD86 surface expression and antigen-presenting function. Autocrine IL-10 sustains MARCH1 expression to continuously ubiquitinate CD86 following LPS activation, and DCs expressing ubiquitination-resistant CD86 (K267 mutant) failed to regulate T cell-activating ability in response to IL-10. MARCH1 knockout mice, ubiquitination-resistant CD86 mutants (K267), functional T cell activation assays, flow cytometry Journal of immunology High 21849678
2005 B7-2 (CD86) exists as a monomer on the cell surface, whereas B7-1 (CD80) is present as a dimer, as demonstrated by FRET-based photobleaching experiments; B7-1 and B7-2 do not form hetero-oligomers with each other on the cell surface. Fluorescence resonance energy transfer (FRET) / photobleaching-based FRET on live cells Immunology letters Medium 16413062
1999 CD86 ligation of CD28 does not induce detectable tyrosine phosphorylation of CD28 itself or robust PI3K association with CD28, nor enhanced PLCγ phosphorylation, whereas CD80 ligation does; however, both CD80 and CD86 activate shared signaling events including CBL and VAV tyrosine phosphorylation, NFAT-dependent transcription, and IL-2 production. CHO cell transfectants expressing CD80 or CD86, anti-CD28 stimulation, immunoprecipitation, Western blot for tyrosine phosphorylation of CD28/PLCγ/PI3K association The Journal of biological chemistry High 9915850
1995 CD28-mediated costimulation by CD86 (B7-2) requires PI3-kinase: CD28 mutants (Y191F and M194C) that selectively disrupted PI3-kinase binding failed to generate IL-2 when co-stimulated with CHO-CD86 cells, directly implicating PI3-kinase in CD86-CD28 signaling leading to IL-2 secretion. CD28 cytoplasmic domain point mutants (Y191F, M194C), CHO cells expressing CD86, IL-2 production assay Immunity High 7584133
1998 Stimulation of CD28 by B7-2 (CD86) leads to rearrangement of the actin cytoskeleton and formation of focal adhesion-like cell contacts, with selective translocation of the Rho-family GTPase Rac1 (but not Rho) to the site of T cell–APC contact, along with talin. F-actin content measurement, confocal microscopy of Rac1/talin localization, T cells co-cultured with B7-2-transfected CHO cells Journal of immunology Medium 9551951
2012 Prohibitin 1 (Phb1) and Prohibitin 2 (Phb2) are transmembrane adaptor proteins that bind to CD86 and cooperate with the CD86 cytoplasmic domain (via PKC phosphorylation sites) to mediate downstream NF-κB signaling in B cells, leading to increased IgG1 expression. Phb1/2 are required for CD86-induced phosphorylation of PLCγ2 and PKCα/β, while both Phb1/2 and the CD86 cytoplasmic domain are required for IκBα phosphorylation. Proteomics-based identification, co-immunoprecipitation, shRNA knockdown of Phb1/2, CD86 cytoplasmic domain truncation/mutation, IgG1 and Oct-2 expression assays Journal of immunology High 23241883
2009 Direct CD86 signaling on B cells (reverse signaling) promotes IgG secretion by previously class-switched B cells and induces expression of XBP-1 and spliced XBP-1, indicating increased protein synthesis; this was demonstrated using mixed bone marrow chimeric mice where only B cells lacked B7-1/B7-2. Mixed bone marrow irradiation chimeras (B cell-specific B7-1/2 deficiency), in vitro CD86 engagement, XBP-1 splicing assay, IgG/IgM ELISA Journal of immunology High 19933871
2004 CD28 signaling in dendritic cells via CD86 (and CD80) induces IL-6 production in a p38 MAPK-dependent manner, and this IL-6 prevents IFN-γ-driven immunosuppressive tryptophan catabolism, demonstrating reverse (bidirectional) signaling through CD86 on DCs. Soluble CD28 treatment of mouse DCs, cytokine measurement, p38 MAPK inhibition, in vivo tumor and microbial challenge models Nature immunology High 15467723
2016 Bacterial superantigens enhance T cell activation by simultaneously binding both CD86 and CD28 at their respective homodimer interfaces (via the same 12-aa β-strand-hinge-α-helix domain), thereby increasing avidity between CD86 and CD28 and driving cytokine hyperproduction; CD86 homodimer interface mimetic peptides block superantigen binding to cell-surface CD86 and attenuate cytokine overproduction. Binding assays, CD86/CD28 dimer interface peptide competition, cytokine assays, in vivo superantigen lethality model Proceedings of the National Academy of Sciences High 27708164
2008 HIV-1 Nef removes CD86 (and CD80) from the cell surface via a clathrin- and dynamin-independent, actin-based endocytic pathway and subsequently reroutes CD86-containing vesicles to the Golgi via a Rab11-dependent mechanism; CD86/CD80 endocytic vesicles do not acquire conventional early endosomal markers (Rab5/EEA1) but instead recruit Rab11 de novo, which is required for Golgi delivery. Fluorescence microscopy, dominant-negative Rab constructs, endosomal marker colocalization, live-cell trafficking assays Traffic High 18764822
2006 Adenovirus serotype 3 (Ad3, species B1) uses CD80 and CD86 as cellular attachment receptors; the Ad fiber-knob domain mediates this interaction, and all tested Ad species B members (B1 and B2) can infect cells through CD80 and CD86. Competitive infection blocking with fiber-knob domain, CHO cells expressing CD80/CD86, serotype-specific infection assays Virus research High 16920215
2017 CD86 (B7.2) functions as a co-receptor for lymphotropic hepatitis C virus (HCV) infection of B cells; cDNA library screening identified CD86 as a B-cell-specific co-receptor, and silencing CD86 prevented HCV infection of B cells. Lymphotropic HCV infection of B cells via CD86 inhibited memory B cell function (recall antigen responses). cDNA library screening, gene silencing of CD86, chimeric HCV infectious clones, B cell infection assays, antigen recall assays Nature communications Medium 28067225
2012 Induced regulatory T cells (iTregs) acquire CD86 (to a greater extent than CD80) from mature dendritic cells via trogocytosis in a CTLA-4-, CD28-, and PD-L1-independent manner; iTregs that acquired CD86 expressed higher activation markers and showed enhanced suppressive capacity compared to iTregs that did not acquire CD86. Co-incubation of CD80/CD86 double-KO-derived iTregs with mature DCs, flow cytometry, confocal fluorescence microscopy, T cell suppression assays Cellular & molecular immunology Medium 22307040
1998 Constitutive expression of a B7.2 transgene on tolerant self-reactive B cells was sufficient to prevent Fas-mediated deletion and trigger T cell-dependent clonal expansion and autoantibody secretion, demonstrating that repression of B7.2 on anergic B cells is a critical mechanism for Fas-mediated peripheral B cell tolerance. B7.2 transgenic mice, in vivo B cell fate tracking, Fas-deficient comparison, T cell-dependent expansion assays The Journal of experimental medicine High 9705947
2011 Toxoplasma gondii induces B7-2 (CD86) expression on macrophages at the transcript level through a mechanism requiring active parasite invasion (not TLR/MyD88/TRIF) and dependent on JNK (but not ERK or p38) MAP kinase signaling; T. gondii-infected macrophages stimulated naïve T cell proliferation in a B7-2-dependent manner. MAPK inhibitors, MyD88/TRIF KO macrophages, B7-2 blocking antibodies, T cell proliferation assays, genome-wide transcriptional analysis Infection and immunity High 21911468
2004 IL-4-dependent upregulation of CD86 in monocytes requires JAK/STAT6 and MEK/ERK1/2 activation but is negatively regulated by PKCδ; blocking JAK with WHI-P154 or MEK with PD98059 abolished CD86 upregulation, while blocking PKCδ with rottlerin dramatically enhanced CD86 expression. Specific kinase inhibitors (WHI-P154, PD98059, rottlerin), STAT6 phosphorylation assays, flow cytometry for CD86, antisense reduction of CD45 Cellular signalling Medium 14636897
2020 Tet2 and Tet3 DNA demethylases in B cells are required for downregulation of CD86 following chronic self-antigen exposure; in Tet2/Tet3-deficient B cells, CD86 remained elevated due to decreased accumulation of HDAC1 and HDAC2 at the Cd86 locus, and anti-CD86 blockade partially restricted the resulting aberrant T and B cell activation. B cell-specific Tet2/Tet3 double-KO mice, HDAC chromatin occupancy (ChIP), anti-CD86 blockade, flow cytometry Nature immunology High 32572241
1997 B7.2 expressed on T cell tumor lines (EL4) preferentially binds CTLA4-Ig but not CD28-Ig and fails to costimulate T cell proliferation (unlike B7.1 on T cells which binds both), suggesting that the context of B7.2 expression affects its receptor binding preference and functional outcome. CTLA4-Ig and CD28-Ig binding assays on B7.1/B7.2 transfected T cell lines, T cell proliferation costimulation assays, in vivo tumor regression Journal of immunology Medium 9036945
1996 The V domain of CD86 (but not the V domain of CD80 alone) is sufficient for CTLA-4 binding, revealing a fundamental structural difference between CD80 and CD86 in receptor engagement. Domain-swapped and truncated CD80/CD86 mutants, binding assays with CTLA-4 Journal of immunology Medium 8609386
2000 HIV-1 virions bearing host-encoded B7-2 activate NF-κB and NFAT in target T cells via CD28 engagement, thereby upregulating HIV-1 LTR-driven gene expression; this effect was abrogated by CTLA-4-Ig blockade of the virion-bound B7-2–CD28 interaction and by dominant-negative IκBα and dnNFAT. Isogenic NL4-3 HIV virus stocks bearing B7-2, dominant-negative transcription factor constructs, CTLA-4-Ig blocking, LTR reporter assays, EMSA for NF-κB The Journal of biological chemistry Medium 11096063
2017 CD86 on myeloma cells signals via its cytosolic domain to promote myeloma cell survival; silencing CD86 (or CD28) leads to myeloma cell death, downregulation of integrins, and downregulation of IRF4 (a known myeloma survival factor), and the pro-survival activity of CD86 is dependent on its cytosolic domain. CD86/CD28 gene silencing (siRNA/shRNA), CD86 cytosolic domain deletion constructs, cell viability assays, IRF4 and integrin expression Blood advances Medium 29296880

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Cellular interaction in germinal centers. Roles of CD40 ligand and B7-2 in established germinal centers. Journal of immunology (Baltimore, Md. : 1950) 379 7541819
1996 Costimulatory molecule-deficient dendritic cell progenitors (MHC class II+, CD80dim, CD86-) prolong cardiac allograft survival in nonimmunosuppressed recipients. Transplantation 306 8830833
2001 Structural basis for co-stimulation by the human CTLA-4/B7-2 complex. Nature 269 11279501
2004 CD28 induces immunostimulatory signals in dendritic cells via CD80 and CD86. Nature immunology 223 15467723
2003 What's the difference between CD80 and CD86? Trends in immunology 221 12810107
2022 Differences in CD80 and CD86 transendocytosis reveal CD86 as a key target for CTLA-4 immune regulation. Nature immunology 171 35999394
2001 Development of spontaneous autoimmune peripheral polyneuropathy in B7-2-deficient NOD mice. The Journal of experimental medicine 169 11535635
1995 Antitumor immunity elicited by tumor cells transfected with B7-2, a second ligand for CD28/CTLA-4 costimulatory molecules. Journal of immunology (Baltimore, Md. : 1950) 144 7533183
1999 CD28/CTLA-4 and CD80/CD86 families: signaling and function. Immunologic research 141 10374692
1995 Preferential dependence of autoantibody production in murine lupus on CD86 costimulatory molecule. European journal of immunology 131 7489744
2001 Histamine induces CD86 expression and chemokine production by human immature dendritic cells. Journal of immunology (Baltimore, Md. : 1950) 123 11342615
1996 B7-2 (CD86) is essential for the development of IL-4-producing T cells. International immunology 120 8921434
1995 Selective CD28pYMNM mutations implicate phosphatidylinositol 3-kinase in CD86-CD28-mediated costimulation. Immunity 118 7584133
2003 Prevention of kidney allograft rejection using anti-CD40 and anti-CD86 in primates. Transplantation 108 12640302
1996 B7-1 but not B7-2 efficiently costimulates CD8+ T lymphocytes in the P815 tumor system in vitro. Journal of immunology (Baltimore, Md. : 1950) 107 8543795
1997 The mucosal adjuvanticity of cholera toxin involves enhancement of costimulatory activity by selective up-regulation of B7.2 expression. Journal of immunology (Baltimore, Md. : 1950) 102 9548469
1995 High-efficiency transfer of the T cell co-stimulatory molecule B7-2 to lymphoid cells using high-titer recombinant adeno-associated virus vectors. Human gene therapy 99 8664378
2011 Ubiquitination of CD86 is a key mechanism in regulating antigen presentation by dendritic cells. Journal of immunology (Baltimore, Md. : 1950) 98 21849678
2019 Local Delivery of Ox40l, Cd80, and Cd86 mRNA Kindles Global Anticancer Immunity. Cancer research 94 30692215
2005 B7-1 and B7-2: similar costimulatory ligands with different biochemical, oligomeric and signaling properties. Immunology letters 94 16413062
2009 B7-1/2 (CD80/CD86) direct signaling to B cells enhances IgG secretion. Journal of immunology (Baltimore, Md. : 1950) 87 19933871
1998 Development of murine allergic asthma is dependent upon B7-2 costimulation. Journal of immunology (Baltimore, Md. : 1950) 86 9551945
2021 CD86+ Antigen-Presenting B Cells Are Increased in Cancer, Localize in Tertiary Lymphoid Structures, and Induce Specific T-cell Responses. Cancer immunology research 84 34155067
1997 Immunomodulatory effects of a plasmid expressing B7-2 on human immunodeficiency virus-1-specific cell-mediated immunity induced by a plasmid encoding the viral antigen. European journal of immunology 80 9079822
1999 NK cell triggering by the human costimulatory molecules CD80 and CD86. Journal of immunology (Baltimore, Md. : 1950) 79 10510357
1999 Anti-CD86 (B7.2) treatment abolishes allergic airway hyperresponsiveness in mice. American journal of respiratory and critical care medicine 78 10228138
1996 Neisserial porins induce B lymphocytes to express costimulatory B7-2 molecules and to proliferate. The Journal of experimental medicine 76 8642257
1996 IFN-alpha induces autoimmune T cells through the induction of intracellular adhesion molecule-1 and B7.2. Journal of immunology (Baltimore, Md. : 1950) 76 8752897
2020 Tet2 and Tet3 in B cells are required to repress CD86 and prevent autoimmunity. Nature immunology 75 32572241
2012 Trogocytosis of CD80 and CD86 by induced regulatory T cells. Cellular & molecular immunology 71 22307040
1998 Repression of B7.2 on self-reactive B cells is essential to prevent proliferation and allow Fas-mediated deletion by CD4(+) T cells. The Journal of experimental medicine 71 9705947
2006 Members of adenovirus species B utilize CD80 and CD86 as cellular attachment receptors. Virus research 65 16920215
2005 Relationship of CD86 surface marker expression and cytotoxicity on dendritic cells exposed to chemical allergen. Toxicology and applied pharmacology 63 15885735
1998 Stimulation of CD28 with B7-2 promotes focal adhesion-like cell contacts where Rho family small G proteins accumulate in T cells. Journal of immunology (Baltimore, Md. : 1950) 63 9551951
1997 Granulocyte-macrophage colony-stimulating factor and B7-2 combination immunogene therapy in an allogeneic Hu-PBL-SCID/beige mouse-human glioblastoma multiforme model. Human gene therapy 63 9189765
1997 B7.2 expressed by T cells does not induce CD28-mediated costimulatory activity but retains CTLA4 binding: implications for induction of antitumor immunity to T cell tumors. Journal of immunology (Baltimore, Md. : 1950) 62 9036945
2001 Differential role of CD80 and CD86 on alveolar macrophages in the presentation of allergen to T lymphocytes in asthma. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 60 11359432
2001 CD40 and CD86 upregulation with divergent CMRF44 expression on blood dendritic cells in inflammatory bowel diseases. The American journal of gastroenterology 60 11693331
1999 CD28 interactions with either CD80 or CD86 are sufficient to induce allergic airway inflammation in mice. American journal of respiratory cell and molecular biology 60 10502560
1998 Upregulation of B7.2, but not B7.1, on B cells from patients with allergic asthma. The Journal of allergy and clinical immunology 58 9449507
1999 CD80 and CD86 are not equivalent in their ability to induce the tyrosine phosphorylation of CD28. The Journal of biological chemistry 57 9915850
2000 Costimulation by B7-1 and B7-2 is required for autoimmune disease in MRL-Faslpr mice. Journal of immunology (Baltimore, Md. : 1950) 56 10820290
1996 Interactions of CD80 and CD86 with CD28 and CTLA4. Journal of immunology (Baltimore, Md. : 1950) 53 8609386
2016 CD80 and CD86 knockdown in dendritic cells regulates Th1/Th2 cytokine production in asthmatic mice. Experimental and therapeutic medicine 52 26998006
1999 Functional expression of costimulatory molecule CD86 on epithelial cells in the inflamed colonic mucosa. Gastroenterology 52 10464129
2013 Circulating CD40+ and CD86+ B cell subsets demonstrate opposing associations with risk of stroke. Arteriosclerosis, thrombosis, and vascular biology 51 24202305
2006 Activation of U937 cells by contact sensitizers: CD86 expression is independent of apoptosis. Journal of immunotoxicology 49 18958700
1996 Requirement of CD80 and CD86 molecules for antigen presentation by eosinophils. Scandinavian journal of immunology 49 8795716
2016 Superantigens hyperinduce inflammatory cytokines by enhancing the B7-2/CD28 costimulatory receptor interaction. Proceedings of the National Academy of Sciences of the United States of America 48 27708164
1998 B7.1 is a quantitatively stronger costimulus than B7.2 in the activation of naive CD8+ TCR-transgenic T cells. Journal of immunology (Baltimore, Md. : 1950) 47 9820499
1995 CD86 (B70/B7-2) on endothelial cells co-stimulates allogeneic CD4+ T cells. International immunology 43 7495740
1997 Regulation of self-tolerance by CD80/CD86 interactions. Current opinion in immunology 42 9492990
1997 B7-2 blockade enhances T cell responses to Leishmania donovani. Journal of immunology (Baltimore, Md. : 1950) 40 9379045
2012 Prohibitins and the cytoplasmic domain of CD86 cooperate to mediate CD86 signaling in B lymphocytes. Journal of immunology (Baltimore, Md. : 1950) 38 23241883
2002 Blockade of CD28/B7-2 costimulation inhibits experimental obliterative bronchiolitis in rat tracheal allografts: suppression of helper T cell type1-dominated immune response. American journal of respiratory and critical care medicine 38 11874822
1997 Characterization of rat CD80 and CD86 by molecular cloning and mAb. International immunology 38 9237108
1995 Role of B70/B7-2 in CD4+ T-cell immune responses induced by dendritic cells. Immunology 38 7558137
2017 Hepatitis C virus has a genetically determined lymphotropism through co-receptor B7.2. Nature communications 37 28067225
2000 Attachment of human immunodeficiency virus-1 (HIV-1) particles bearing host-encoded B7-2 proteins leads to nuclear factor-kappa B- and nuclear factor of activated T cells-dependent activation of HIV-1 long terminal repeat transcription. The Journal of biological chemistry 37 11096063
1997 Functional CD86 (B7-2/B70) is predominantly expressed on Langerhans cells in atopic dermatitis. The British journal of dermatology 37 9217814
2014 Small interfering RNA against CD86 during allergen challenge blocks experimental allergic asthma. Respiratory research 36 25344652
2002 Human plasma contains a soluble form of CD86 which is present at elevated levels in some leukaemia patients. Leukemia 36 11986949
1998 Effects of in vivo administration of anti-B7-1/B7-2 monoclonal antibodies on murine acute myocarditis caused by coxsackievirus B3. Circulation research 36 9529166
2011 Toxoplasma gondii induces B7-2 expression through activation of JNK signal transduction. Infection and immunity 35 21911468
2001 IL-3 induces B7.2 (CD86) expression and costimulatory activity in human eosinophils. Journal of immunology (Baltimore, Md. : 1950) 35 11714768
2013 CD86 is an activation receptor for NK cell cytotoxicity against tumor cells. PloS one 34 24349559
2005 CD80 and CD86 costimulatory molecules regulate crescentic glomerulonephritis by different mechanisms. Kidney international 34 16014035
1996 Functional CD86 (B7-2/B70) on cultured human Langerhans cells. The Journal of investigative dermatology 34 8592066
2005 Upregulation of CD40, CD80, CD83 or CD86 on alveolar macrophages after lung transplantation. The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation 33 16102442
2004 Clinical significance of costimulatory molecules CD80/CD86 expression in IgA nephropathy. Kidney international 33 14871408
1997 T cell-mediated elimination of B7.2 transgenic B cells. Immunity 33 9075933
2021 Pomalidomide restores immune recognition of primary effusion lymphoma through upregulation of ICAM-1 and B7-2. PLoS pathogens 30 33411730
2009 Preferential use of B7.2 and not B7.1 in priming of vaccinia virus-specific CD8 T cells. Journal of immunology (Baltimore, Md. : 1950) 30 19234186
2008 HIV-1 Nef induces a Rab11-dependent routing of endocytosed immune costimulatory proteins CD80 and CD86 to the Golgi. Traffic (Copenhagen, Denmark) 30 18764822
2005 Evaluation of CD86 gene polymorphism at +1057 position in liver transplant recipients. Transplant immunology 30 16223675
2003 Recovery from EAE is associated with decreased survival of encephalitogenic T cells in the CNS of B7-1/B7-2-deficient mice. European journal of immunology 30 12884869
1998 Expression and co-stimulatory function of B7-2 on murine CD4+ T cells. European journal of immunology 30 9541581
2020 Bacteroides fragilis alleviates the symptoms of lupus nephritis via regulating CD1d and CD86 expressions in B cells. European journal of pharmacology 29 32721450
2005 CD86 and beta2-adrenergic receptor stimulation regulate B-cell activity cooperatively. Trends in immunology 28 15797507
2004 B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. Journal of immunology (Baltimore, Md. : 1950) 28 15356107
2011 CD86 + 1057G/A polymorphism and susceptibility to osteosarcoma. DNA and cell biology 27 21563968
2007 Targeting adenovirus to CD80 and CD86 receptors increases gene transfer efficiency to malignant glioma cells. Journal of neurosurgery 27 17886563
2009 Functional B7.2 and B7-H2 molecules on myeloma cells are associated with a growth advantage. Clinical cancer research : an official journal of the American Association for Cancer Research 26 19188146
2007 Reduced monocyte CD86 expression in postinflammatory immunodeficiency. Critical care medicine 26 17204999
2004 Soluble CD86 protein in serum samples of patients with asthma. Thorax 26 15454653
2008 B7-1 and B7-2 differentially control peripheral homeostasis of CD4(+)CD25(+)Foxp3(+) regulatory T cells. Transplant immunology 25 18848987
2004 IL-4-dependent CD86 expression requires JAK/STAT6 activation and is negatively regulated by PKCdelta. Cellular signalling 25 14636897
2004 Chronic ethanol ingestion by mice increases expression of CD80 and CD86 by activated macrophages. Alcohol (Fayetteville, N.Y.) 25 15163560
2003 Cross-species costimulation: relative contributions of CD80, CD86, and CD40. Transplantation 25 12829914
2002 Blocking the CD80 and CD86 costimulation molecules: lessons to be learned from animal models. Transplantation 25 11810057
1998 Human melanoma cells transfected with the B7-2 co-stimulatory molecule induce tumor-specific CD8+ cytotoxic T lymphocytes in vitro. Human gene therapy 25 9650618
1996 Therapeutic effectiveness of the immunity elicited by P815 tumor cells engineered to express the B7-2 costimulatory molecule. Cancer immunology, immunotherapy : CII 25 8640844
1998 Costimulatory molecules (CD80 and CD86) on Reed-Sternberg cells are associated with the proliferation of background T cells in Hodgkin's disease. Pathology international 24 9589458
1997 Expression of B7-2 (CD86) molecules by Reed-Sternberg cells of Hodgkin's disease. Leukemia 24 9177439
2007 A functional CD86 polymorphism associated with asthma and related allergic disorders. Journal of medical genetics 23 17513529
2014 AID induces intraclonal diversity and genomic damage in CD86(+) chronic lymphocytic leukemia cells. European journal of immunology 22 25179679
2010 Rhipicephalus microplus salivary gland molecules induce differential CD86 expression in murine macrophages. Parasites & vectors 21 21054882
1999 B7-2 is required for the progression but not the initiation of the type 2 immune response to a gastrointestinal nematode parasite. Journal of immunology (Baltimore, Md. : 1950) 21 10201938
1995 Effect of CD80 and CD86 on T cell cytokine production. Immunological investigations 21 8575841
2017 CD86 regulates myeloma cell survival. Blood advances 20 29296880