Affinage

BTN3A1

Butyrophilin subfamily 3 member A1 · UniProt O00481

Length
513 aa
Mass
57.7 kDa
Annotated
2026-06-09
38 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 4/5 claims corpus-supported (80%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BTN3A1 (CD277) is a type-I transmembrane butyrophilin that operates as an intracellular phosphoantigen (pAg) sensor required for activation of Vγ9Vδ2 T cells (PMID:22767497, PMID:22846996). Sensing occurs through its cytoplasmic B30.2 domain, which directly binds pAgs in a positively charged surface pocket—microbial HMBPP with high affinity and endogenous IPP with lower affinity—and discriminates antigenic from non-antigenic phosphometabolites by their ability to trigger a conformational change that propagates from the binding pocket to distal regions of the domain (PMID:25637025, PMID:28807997, PMID:28862425). pAg binding does not act alone: HMBPP bridges the B30.2 domain of BTN3A1 to that of BTN2A1, forming a cytoplasmic BTN2A1–BTN3A1 complex within a larger BTN3A1–BTN3A2–BTN2A1 assembly, and these intracellular events are relayed to the cell surface through the BTN3A1 juxtamembrane region and a membrane-proximal di-leucine motif that recruits periplakin, both of which are required for T cell triggering (PMID:37171180, PMID:25637025, PMID:28461569). Surface signal output requires reorganization of the extracellular V-shaped homodimers and juxtamembrane phosphorylation-dependent BTN2A1–BTN3A1 heterodimerization, with BTN2A1 and BTN3A2 ectodomains engaging distinct surfaces of the Vγ9Vδ2 TCR in an inside-out 'gripping' mechanism [PMID:28807997, PMID:bio_10.1101_2024.10.02.616253]. Beyond γδ T cell triggering, BTN3A1 on tumor cells suppresses αβ T cell activation by preventing exclusion of N-glycosylated CD45 from the immune synapse (PMID:32820120), acts as a positive regulator of nucleic-acid-induced type I interferon signaling by constitutively associating with TBK1 and undergoing dynein/MAP4-dependent perinuclear redistribution to promote TBK1–IRF3 phosphorylation (PMID:27911820), and is transcriptionally induced by HIF-1α to drive ULK1-mediated autophagy and radioresistance in esophageal carcinoma (PMID:36418890). Its transcription is controlled by NLRC5 and HIF-1α (PMID:33364588, PMID:36418890).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2012 High

    Established that the BTN3A1 isoform specifically, not other CD277 isoforms, is the molecule required for phosphoantigen-induced Vγ9Vδ2 T cell activation, and linked pAg sensing to changes in BTN3A1 membrane behavior.

    Evidence CD277 knockdown, domain-shuffling, FRAP, and functional agonist/antagonist antibody assays

    PMID:22767497

    Open questions at the time
    • Did not identify where pAg binds within BTN3A1
    • Did not resolve the molecular link between altered membrane mobility and TCR engagement
  2. 2012 High

    Defined the resting architecture of BTN3A as V-shaped homodimers associating through their membrane-proximal Ig domains, and localized agonist/antagonist antibody epitopes to the Ig-V domain.

    Evidence X-ray crystallography and antibody binding plus functional T cell assays

    PMID:22846996

    Open questions at the time
    • Did not address how ectodomain conformation couples to intracellular sensing
    • No structure of the full-length receptor or its partners
  3. 2014 High

    Distinguished antibody-mediated from pAg-mediated activation, showing BTN3A1 alone suffices for agonist-antibody triggering but pAg sensing requires additional chromosome-6-encoded gene(s).

    Evidence Genetic complementation comparing BTN3A1-transduced CHO cells with cells carrying human chromosome 6, across multiple TCR transductants

    PMID:24890657

    Open questions at the time
    • The required cofactor gene(s) on chromosome 6 were not identified here
  4. 2015 High

    Provided the direct biochemical basis for sensing by showing pAgs bind the intracellular B30.2 domain and identifying periplakin as a cytoplasmic-tail partner functionally required for γδ activation.

    Evidence In vitro B30.2 binding assays, yeast two-hybrid, co-IP, and knockdown/re-expression rescue with functional T cell assays

    PMID:25637025

    Open questions at the time
    • Did not show how B30.2 occupancy is transmitted to the membrane or to the TCR
    • Mechanistic role of periplakin beyond binding not resolved
  5. 2016 High

    Revealed a distinct innate-immune function: BTN3A1 constitutively binds TBK1 and undergoes MAP4/dynein-dependent perinuclear relocation to bridge TBK1–IRF3 and drive type I interferon signaling.

    Evidence Reciprocal co-IP, BTN3A1 and MAP4 knockdown, subcellular fractionation/immunofluorescence, and IFN-β reporter assays

    PMID:27911820

    Open questions at the time
    • How nucleic-acid sensing triggers BTN3A1 redistribution is unresolved
    • Relationship between this innate role and pAg sensing is not addressed
  6. 2016 Medium

    Supported the inside-out model by demonstrating that intracellular delivery of HMBPP into target cells is required for BTN3A1-dependent lysis.

    Evidence Cytotoxicity assays with temperature-dependent uptake block and a cell-permeable prodrug bypass

    PMID:27271567

    Open questions at the time
    • Indirect inference of intracellular sensing from uptake manipulation
    • Did not directly visualize intracellular pAg-BTN3A1 engagement
  7. 2017 High

    Defined the sensing mechanism as conformational: pAg binding induces a global B30.2 conformational change, and locking the ectodomain V-shape blunts activation, tying intracellular sensing to extracellular reorganization.

    Evidence NMR, X-ray crystallography, MD simulations, and cellular T cell activation assays (two studies)

    PMID:28807997 PMID:28862425

    Open questions at the time
    • How the B30.2 conformational change propagates across the membrane was not established
    • Identity of the surface partner transmitting the signal not yet known
  8. 2017 Medium

    Identified the juxtamembrane domain as a critical transmission element, with mutations bidirectionally tuning γδ T cell reactivity.

    Evidence Domain mutagenesis with functional T cell activation assays

    PMID:28461569

    Open questions at the time
    • The interacting partner at the juxtamembrane interface was not defined here
    • Single-lab mutagenesis without structural confirmation of the proposed dimerization interface
  9. 2019 Medium

    Mapped B30.2 ligand-binding determinants (notably H381) and showed that binding affinity and antigenic potency are not linearly correlated, reinforcing the conformational-sensor model.

    Evidence Site-directed mutagenesis, fluorescence-polarization binding, T cell proliferation/IFN-γ assays, and docking

    PMID:31268699

    Open questions at the time
    • Did not resolve what distinguishes activating from non-activating bound conformations structurally
  10. 2020 High

    Uncovered a tumor-immunosuppressive function whereby BTN3A1 inhibits αβ TCR activation by preventing CD45 segregation from the immune synapse, while anti-CD277 restores αβ responses and elicits BTN2A1-dependent γδ cytotoxicity.

    Evidence Co-culture T cell assays, immune synapse imaging, BTN3A1 expression manipulation, and in vivo tumor models

    PMID:32820120

    Open questions at the time
    • Molecular basis of CD45 retention by BTN3A1 not detailed
    • Relationship to the γδ-activating function in the same synapse not fully integrated
  11. 2020 Medium

    Placed BTN3A transcription downstream of NLRC5, linking antigen-presentation regulation to γδ-mediated tumor killing.

    Evidence Promoter reporter assays, NLRC5 OE/KD, and BTN3A-dependent T cell cytotoxicity assays

    PMID:33364588

    Open questions at the time
    • The atypical promoter motif's direct occupancy mechanism not biochemically resolved
  12. 2022 Medium

    Identified a cancer-intrinsic role in which HIF-1α-induced BTN3A1 binds ULK1 and promotes its phosphorylation to drive autophagy-mediated radioresistance.

    Evidence Co-IP/mass spectrometry, ChIP, luciferase reporter, and KD/OE in vitro and in vivo in esophageal carcinoma

    PMID:36418890

    Open questions at the time
    • Whether BTN3A1 directly catalyzes or scaffolds ULK1 phosphorylation is unclear
    • Relationship to BTN3A1's immune functions not addressed
  13. 2023 High

    Demonstrated the molecular partnership underlying pAg relay: HMBPP binds BTN3A1 (not BTN2A1) and bridges a cytoplasmic BTN2A1–BTN3A1 complex dependent on BTN2A1 B30.2 homodimerization.

    Evidence 31P-NMR, NMR, ITC, size-exclusion chromatography, and mutagenesis (L325G) with functional T cell ELISA

    PMID:37171180

    Open questions at the time
    • Stoichiometry within the full receptor assembly not resolved here
    • How the cytoplasmic complex couples to surface TCR engagement not shown
  14. 2024 Low

    Linked surface heterodimerization to activation, showing that juxtamembrane phosphorylation of BTN3A1 drives BTN2A1–BTN3A1 surface heterodimerization required for full Vγ9Vδ2 TCR activation, and identified PHLDB2, SYNJ2, and CARMIL1 as regulators.

    Evidence Step-wise mutagenesis organoid/cell models, surface expression analysis, interactome mapping, and T cell assays (preprint)

    PMID:bio_10.1101_2024.11.19.624272

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • The responsible juxtamembrane kinase is not identified
    • Mechanistic roles of PHLDB2/SYNJ2/CARMIL1 not defined
  15. 2024 Medium

    Provided structural integration of the full pathway, showing HMBPP-bridged intracellular B30.2 contacts and a 'pliers-like' ectodomain rearrangement engaging the Vγ9Vδ2 TCR.

    Evidence Cryo-EM of full-length BTN3A1–BTN3A2–BTN2A1 complexes (preprint)

    PMID:bio_10.1101_2024.10.02.616253

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Dynamics of the inside-out transition between resting and engaged states not captured
  16. 2024 Medium

    Extended the tumor-immune role by showing tumor BTN3A1 drives Vγ9Vδ2 T cell exhaustion via TCR-dependent NR4A2/3 induction within an IFN-γ feedback loop upregulating BTN3A1 and PD-L1.

    Evidence BTN3A1 KO/OE in tumor lines, co-culture with Vδ2 T cells, RNA-seq, flow cytometry, and NR4A2/3 knockdown rescue

    PMID:39342337

    Open questions at the time
    • Causal contribution of the IFN-γ feedback loop in vivo not fully established
    • Generalizability beyond cervical cancer not tested
  17. 2025 Medium

    Refined the conformational map, using 19F NMR to localize HMBPP/BTN2A1-induced changes to the B30.2 domain and to a BTN2A1-binding interface residue (W421), while juxtamembrane residues remain unaffected.

    Evidence 19F solution NMR of point mutants with binding affinity measurements

    PMID:40079188

    Open questions at the time
    • Single method type
    • How the larger B30.2 conformational change is mechanically transmitted not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the intracellular B30.2 conformational change and BTN2A1 complex are mechanically transduced across the membrane to drive surface heterodimerization, and which kinase phosphorylates the BTN3A1 juxtamembrane region.
  • No identified juxtamembrane kinase
  • No peer-reviewed full-length structure of resting versus TCR-engaged states
  • Integration of BTN3A1's γδ-sensing, αβ-suppressive, interferon, and autophagy roles is incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140299 molecular sensor activity 4 GO:0008289 lipid binding 2 GO:0060089 molecular transducer activity 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0005829 cytosol 3 GO:0005886 plasma membrane 3
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3 R-HSA-9612973 Autophagy 1
Partners
BTN2A1BTN3A2IRF3MAP4PERIPLAKINTBK1ULK1
Complex memberships
BTN3A1-BTN3A2-BTN2A1 receptor complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 BTN3A1 (CD277) is required for phosphoantigen (PAg)-induced Vγ9Vδ2 T cell activation; CD277 knockdown and domain-shuffling confirmed the BTN3A1 isoform is specifically implicated. FRAP experiments showed that intracellular PAg accumulation decreases BTN3A1 membrane mobility, linking PAg sensing to altered membrane dynamics. CD277 knockdown, domain-shuffling, FRAP, antibody agonist/antagonist functional assays Blood High 22767497
2012 The three BTN3A isoforms (BTN3A1, BTN3A2, BTN3A3) exist as V-shaped homodimers in solution, associating through the membrane-proximal C-type Ig domain. The agonist antibody 20.1 and antagonist antibody 103.2 bind separate epitopes on the BTN3A Ig-V domain with high affinity but different valencies. BTN3A1 is necessary for Vγ9Vδ2 T cell activation. X-ray crystallography, structural studies, antibody binding assays, functional T cell activation assays The Journal of biological chemistry High 22846996
2015 Phosphoantigens bind directly to the intracellular B30.2 domain of BTN3A1: microbial HMBPP binds with affinity ~1.1 µM and endogenous IPP at ~627 µM. The plakin family member periplakin interacts with a membrane-proximal di-leucine motif in the BTN3A1 cytoplasmic tail; this interaction is functionally required for γδ T cell activation (re-expression of BTN3A1 lacking the periplakin binding motif fails to restore responses). In vitro binding assay (B30.2 domain), yeast two-hybrid, co-IP, knockdown/re-expression rescue, functional T cell activation assays Journal of immunology High 25637025
2017 Phosphoantigen binding to the intracellular B30.2 domain of BTN3A1 induces a global conformational change in that domain, as characterized by NMR and MD simulations. Two distinct dimer interfaces in the full-length intracellular domain are near the pAg-binding pocket. The extracellular domains of BTN3A1 adopt a V-shaped conformation at rest; locking them in this conformation (without perturbing membrane reorganization) diminishes pAg-induced T cell activation. NMR spectroscopy, X-ray crystallography, molecular dynamics simulations, biochemical assays, cellular T cell activation assays Proceedings of the National Academy of Sciences of the United States of America High 28807997
2017 The BTN3A1 B30.2 domain binds phosphoantigens and various negatively charged small molecules in a positively charged surface pocket. BTN3A1 discriminates phosphoantigens from non-antigenic small molecules by their ability to induce a specific conformational change propagating from the pAg binding site to distal parts of the domain, acting as a conformational antigenic sensor. NMR chemical shift perturbation, X-ray crystallography ACS chemical biology High 28862425
2017 The juxtamembrane domain of BTN3A1 is required for correct pAg-induced Vγ9Vδ2 T cell activation; mutations in the juxtamembrane domain (but not the transmembrane domain) markedly enhanced or reduced γδ T cell reactivity. A juxtamembrane region identified as a possible dimerization interface proximal to the B30.2 domain is particularly important. Domain mutagenesis, functional T cell activation assays Journal of immunology Medium 28461569
2016 BTN3A1 acts as a positive regulator of nucleic acid-mediated type I interferon signaling. In the resting state, BTN3A1 is constitutively associated with TBK1. Upon nucleic acid stimulation, the BTN3A1-TBK1 complex redistributes to the perinuclear region where BTN3A1 mediates the interaction between TBK1 and IRF3, leading to IRF3 phosphorylation. Microtubule-associated protein MAP4 controls dynein-dependent transport of BTN3A1 to the perinuclear region in response to nucleic acid stimulation. Co-immunoprecipitation, knockdown (BTN3A1 and MAP4), subcellular fractionation/localization, IFN-β reporter assays, immunofluorescence Proceedings of the National Academy of Sciences of the United States of America High 27911820
2014 BTN3A1 expression alone is sufficient for activation of Vγ9Vδ2 T cells by the agonist antibody 20.1, but PAg-mediated Vγ9Vδ2 T cell activation requires BTN3A1 plus additional gene(s) on human chromosome 6. Genetic complementation — BTN3A1 transduction into CHO cells vs. CHO cells containing entire human chromosome 6; Vγ9Vδ2 TCR transductant activation assays European journal of immunology High 24890657
2016 Internalization of HMBPP into target cells is required for BTN3A1-dependent lysis by Vγ9Vδ2 effector T cells (pretreatment at 4°C decreased HMBPP-induced lysis). A cell-permeable prodrug that bypasses energy-dependent uptake restores BTN3A1-dependent lysis, supporting an inside-out model of T cell triggering by intracellular BTN3A1. Cytotoxicity assays, temperature-dependent uptake experiments, BTN3A1 disruption, prodrug/compound comparison Journal of immunology Medium 27271567
2019 Site-directed mutagenesis of BTN3A1 B30.2 domain identified H381 as critical for ligand binding (mutation fully blocks binding), while mutations to charged surface residues impacted diphosphate interactions. Monophosphonate analogs bind similarly to BTN3A1 but differ in antigenicity, demonstrating that BTN3A1 binding and T cell activation efficacy are not linearly correlated. Site-directed mutagenesis, fluorescence polarization binding assay, T cell proliferation and IFN-γ assays, molecular docking Journal of medicinal chemistry Medium 31268699
2020 BTN3A1 on tumor cells inhibits tumor-reactive αβ T cell receptor activation by preventing segregation of N-glycosylated CD45 from the immune synapse. CD277-specific antibodies restore αβ T cell effector activity and elicit BTN2A1-dependent γδ lymphocyte cytotoxicity against BTN3A1+ cancer cells. In vitro co-culture T cell activation assays, immune synapse imaging, BTN3A1 expression manipulation, in vivo tumor models Science High 32820120
2022 BTN3A1 promotes radioresistance in esophageal squamous cell carcinoma by activating ULK1-mediated autophagy; BTN3A1 interacts with ULK1 (identified by immunoprecipitation and mass spectrometry) and promotes ULK1 phosphorylation to initiate autophagy. HIF-1α directly promotes BTN3A1 transcription upon irradiation (confirmed by ChIP and luciferase reporter assay). Immunoprecipitation, mass spectrometry, western blotting, ChIP, luciferase reporter assay, KD/OE in vitro and in vivo Cell death & disease Medium 36418890
2020 NLRC5 promotes transcription of BTN3A1-3 genes through an atypical regulatory motif in their promoters. Forced NLRC5 expression promoted Vγ9Vδ2 T cell-mediated killing of tumor cells in a BTN3A-dependent manner. Promoter reporter assays, gene expression manipulation (OE/KD), T cell cytotoxicity assays, correlation analysis in primary cells iScience Medium 33364588
2011 T cells express all three BTN3/CD277 isoforms, whereas NK cells express mostly BTN3A2 (which lacks the B30.2 intracellular domain). BTN3A1 triggering on T cells enhances TCR-induced signaling; however, BTN3A1 triggering does not affect NK cell activation, while specific engagement of BTN3A2 (but not BTN3A1) decreases NKp30-induced cytokine production. Isoform-specific expression analysis, functional antibody triggering assays, cytokine/proliferation measurements, TCR signaling assays European journal of immunology Medium 21918970
2023 HMBPP binds to the B30.2 domain of BTN3A1 but not to BTN2A1 (confirmed by 31P-NMR, abrogating signals from both phosphorus atoms upon BTN3A1 binding). The BTN2A1 B30.2 domain forms a homodimer; mutation L325G (but not L318G) both prevents BTN2A1 internal domain homodimerization and blocks its binding to HMBPP-bound BTN3A1 (measured by ITC), identifying a cytoplasmic BTN2A1-BTN3A1/HMBPP complex. 31P-NMR, size exclusion chromatography, NMR, isothermal titration calorimetry (ITC), site-directed mutagenesis, functional T cell ELISA assays Journal of immunology High 37171180
2025 19F NMR of specific BTN3A1 point mutants (W421C, T449C, T506C) showed these residues are conformationally influenced by HMBPP and BTN2A1 association. W421 is at the BTN2A1 binding interface (19F labeling of W421C reduces BTN2A1 binding affinity). T506 is distal from the pAg binding site, indicating a larger conformational change in the B30.2 domain upon HMBPP and BTN2A1 binding. Juxtamembrane residues T304C and G323C are unaffected, localizing changes to the B30.2 domain. 19F solution NMR, site-directed mutagenesis, binding affinity measurements FASEB journal Medium 40079188
2024 Cryo-EM structures show that HMBPP bridges the intracellular B30.2 domains of BTN3A1 and BTN2A1 within the full-length BTN3A1-BTN3A2-BTN2A1 complex. Upon Vγ9Vδ2 TCR engagement, BTN3A2-BTN2A1 ectodomain interaction dissociates: BTN2A1 binds the lateral surface of the Vγ9 chain and BTN3A2 binds the apical surface of the Vδ2 chain, suggesting a 'pliers-like gripping' mechanism for TCR activation. Cryo-electron microscopy (cryo-EM) structural determination of full-length complexes bioRxivpreprint Medium bio_10.1101_2024.10.02.616253
2024 BTN3A1 expressed on cervical cancer cells promotes Vγ9Vδ2 T cell exhaustion by engaging γδ TCRs and upregulating transcription factors NR4A2/3 downstream of TCR signaling. Blocking TCR or knocking down NR4A2/3 reverses BTN3A1-induced T cell exhaustion. IFN-γ secreted by Vδ2 T cells in turn promotes BTN3A1 and PD-L1 expression on tumor cells (a feedback loop). BTN3A1 KO/OE in tumor cell lines, co-culture with Vδ2 T cells, flow cytometry, RNA-seq, Western blot, gene knockdown Cell communication and signaling Medium 39342337
2025 ICT01 (agonist antibody targeting BTN3A extracellular domain) binds to a unique region in the BTN3A extracellular domain, destabilizes the BTN2A1-BTN3A interface, and facilitates Vγ9Vδ2 TCR engagement, resulting in γδ T cell activation independently of phosphoantigens. Structural analysis, biochemical assays, cellular T cell activation assays bioRxivpreprint Low bio_10.1101_2025.10.21.681109
2024 Full activation of Vγ9Vδ2 TCR requires phosphorylation of juxtamembrane (JTM) amino acids of BTN3A1, leading to activating heterodimerization of BTN2A1 and BTN3A1 at the cell surface. Single oncogenic mutations in cells upregulate surface BTN2A1 and enable Vγ9Vδ2 TCR binding, but full T cell activation additionally requires BTN3A1 JTM phosphorylation-dependent heterodimerization. PHLDB2, SYNJ2, and CARMIL1 were identified as key regulators of this surface heterodimerization. Step-wise mutagenesis organoid/cell models, surface BTN2A1/3A1 expression analysis, protein interactome mapping, in vitro and in vivo T cell activation assays bioRxivpreprint Low bio_10.1101_2024.11.19.624272

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Key implication of CD277/butyrophilin-3 (BTN3A) in cellular stress sensing by a major human γδ T-cell subset. Blood 484 22767497
2012 The molecular basis for modulation of human Vγ9Vδ2 T cell responses by CD277/butyrophilin-3 (BTN3A)-specific antibodies. The Journal of biological chemistry 147 22846996
2020 BTN3A1 governs antitumor responses by coordinating αβ and γδ T cells. Science (New York, N.Y.) 131 32820120
2015 Activation of human γδ T cells by cytosolic interactions of BTN3A1 with soluble phosphoantigens and the cytoskeletal adaptor periplakin. Journal of immunology (Baltimore, Md. : 1950) 128 25637025
2017 Phosphoantigen-induced conformational change of butyrophilin 3A1 (BTN3A1) and its implication on Vγ9Vδ2 T cell activation. Proceedings of the National Academy of Sciences of the United States of America 105 28807997
2014 Vγ9Vδ2 TCR-activation by phosphorylated antigens requires butyrophilin 3 A1 (BTN3A1) and additional genes on human chromosome 6. European journal of immunology 71 24890657
2011 Differential role for CD277 as a co-regulator of the immune signal in T and NK cells. European journal of immunology 70 21918970
2020 Baseline plasma levels of soluble PD-1, PD-L1, and BTN3A1 predict response to nivolumab treatment in patients with metastatic renal cell carcinoma: a step toward a biomarker for therapeutic decisions. Oncoimmunology 61 33178494
2017 BTN3A1 Discriminates γδ T Cell Phosphoantigens from Nonantigenic Small Molecules via a Conformational Sensor in Its B30.2 Domain. ACS chemical biology 59 28862425
2017 Butyrophilin 3A (BTN3A, CD277)-specific antibody 20.1 differentially activates Vγ9Vδ2 TCR clonotypes and interferes with phosphoantigen activation. European journal of immunology 53 28386905
2016 Butyrophilin 3A/CD277-Dependent Activation of Human γδ T Cells: Accessory Cell Capacity of Distinct Leukocyte Populations. Journal of immunology (Baltimore, Md. : 1950) 42 27619996
2016 HMBPP Analog Prodrugs Bypass Energy-Dependent Uptake To Promote Efficient BTN3A1-Mediated Malignant Cell Lysis by Vγ9Vδ2 T Lymphocyte Effectors. Journal of immunology (Baltimore, Md. : 1950) 41 27271567
2017 The Juxtamembrane Domain of Butyrophilin BTN3A1 Controls Phosphoantigen-Mediated Activation of Human Vγ9Vδ2 T Cells. Journal of immunology (Baltimore, Md. : 1950) 39 28461569
2016 MAP4-regulated dynein-dependent trafficking of BTN3A1 controls the TBK1-IRF3 signaling axis. Proceedings of the National Academy of Sciences of the United States of America 29 27911820
2022 Up-regulation of BTN3A1 on CD14+ cells promotes Vγ9Vδ2 T cell activation in psoriasis. Proceedings of the National Academy of Sciences of the United States of America 23 36288286
2022 BTN3A1 promotes tumor progression and radiation resistance in esophageal squamous cell carcinoma by regulating ULK1-mediated autophagy. Cell death & disease 23 36418890
2020 NLRC5 promotes transcription of BTN3A1-3 genes and Vγ9Vδ2 T cell-mediated killing. iScience 23 33364588
2022 Cutting Edge: Bispecific γδ T Cell Engager Containing Heterodimeric BTN2A1 and BTN3A1 Promotes Targeted Activation of Vγ9Vδ2+ T Cells in the Presence of Costimulation by CD28 or NKG2D. Journal of immunology (Baltimore, Md. : 1950) 22 36096643
2021 Comprehensive analysis of BTN3A1 in cancers: mining of omics data and validation in patient samples and cellular models. FEBS open bio 20 34293829
2018 Regulation of Human γδ T Cells by BTN3A1 Protein Stability and ATP-Binding Cassette Transporters. Frontiers in immunology 18 29670629
2018 ABCA1, apoA-I, and BTN3A1: A Legitimate Ménage à Trois in Dendritic Cells. Frontiers in immunology 17 29937767
2021 Long noncoding RNA HOXA-AS2 accelerates cervical cancer by the miR-509-3p/BTN3A1 axis. The Journal of pharmacy and pharmacology 14 34240204
2019 Probing the Ligand-Binding Pocket of BTN3A1. Journal of medicinal chemistry 11 31268699
2024 BTN3A1 expressed in cervical cancer cells promotes Vγ9Vδ2 T cells exhaustion through upregulating transcription factors NR4A2/3 downstream of TCR signaling. Cell communication and signaling : CCS 10 39342337
2023 Mutations to the BTN2A1 Linker Region Impact Its Homodimerization and Its Cytoplasmic Interaction with Phospho-Antigen-Bound BTN3A1. Journal of immunology (Baltimore, Md. : 1950) 9 37171180
2022 Synthesis and Metabolism of BTN3A1 Ligands: Studies on Diene Modifications to the Phosphoantigen Scaffold. ACS medicinal chemistry letters 8 35178171
2022 CD277 agonist enhances the immunogenicity of relapsed/refractory acute myeloid leukemia towards Vδ2+ T cell cytotoxicity. Annals of hematology 7 35920929
2023 Synergistic effects of BTN3A1, SHP2, CD274, and STAT3 gene polymorphisms on the risk of systemic lupus erythematosus: a multifactorial dimensional reduction analysis. Clinical rheumatology 5 37688767
2022 Elevated Expressions of BTN3A1 and RhoB in Psoriasis Vulgaris Lesions by an Immunohistochemical Study. Applied immunohistochemistry & molecular morphology : AIMM 5 34545848
2025 Autologous Peripheral Vγ9Vδ2 T Cell Synergizes with αβ T Cell Through Antigen Presentation and BTN3A1 Blockade in Immunotherapy of Cervical Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 4 40091603
2017 A Photo-Crosslinkable Biotin Derivative of the Phosphoantigen (E)-4-Hydroxy-3-Methylbut-2-Enyl Diphosphate (HMBPP) Activates Vγ9Vδ2 T Cells and Binds to the HMBPP Site of BTN3A1. Chemistry (Weinheim an der Bergstrasse, Germany) 4 28631855
2025 BTN2A1 and BTN3A1 as Novel Coeliac Disease Risk Loci: An In Silico Analysis. International journal of molecular sciences 2 41226733
2020 [Butyrophilin 3A1 (BTN3A1) enhances activation and proliferation of human peripheral blood Vγ9Vδ2 T cells induced by MTB-HAg]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 2 32958123
2017 BTN3A1-antibodies and phosphoantigens: TCRVγ9Vδ2 "see" the difference. European journal of immunology 2 28597565
2024 A regulatory variant rs9379874 in T1D risk region 6p22.2 affects BTN3A1 expression regulating T cell function. Acta diabetologica 1 39417845
2026 Metformin sensitizes esophageal squamous cell carcinoma to Vγ9Vδ2 T cell-mediated cytotoxicity by upregulating BTN3A1 and BTN2A1. Cell death & disease 0 42248853
2025 Synthesis and evaluation of triazole-containing aryl/acyloxy prodrugs of a BTN3A1 ligand. European journal of medicinal chemistry 0 39919440
2025 Investigation of structural and dynamic properties of the Butyrophilin BTN3A1/BTN2A1 cytoplasmic complex by 19F solution NMR. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 40079188

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