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Elabscience Biotechnology cd4 apc
Cd4 Apc, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+cd4/APC+Anti-Mouse+CD4+Antibody/pm42909153-503-21-23
Average 94 stars, based on 42 article reviews

cd4 apc - by Bioz Stars, 2026-11

94/100 stars

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Staining:

Article Title: Helminth reshapes host gut microbiota and immunoregulation by deploying an antimicrobial program of innate immunity
Article Snippet: .. Briefly, the cells were stained with antibodies of Fixable Viability Dye (Cat. 65-0866-14, eBioscience, 1 μL/mL) for dead cells, and anti-CD16/32 mAbs (Cat. E-AB-F0997A, eBioscience, 10 μg/mL) to block Fc receptors, followed by staining with antibodies against surface markers, including anti-CD3 (Cat. E-AB-F1013J, eBioscience, 50 μL/mL), and anti-CD4 (Cat. E-AB-F1097S, Elabscience, 50 μL/mL). .. For intracellular markers, cells were fixed and permeabilized using a Fixation/Permeabilization kit (Cat.00-5123-43, Invitrogen, 1:3 dilution) and stained for anti-FoxP3 (Cat, E-AB-F1238D, Elabscience, 50 μL/mL) and anti-Helios (Cat. 11-9883-82, eBioscience, 2.5 μg/mL) at 4°C for 1 h. The results were analyzed on a flow cytometer (Coulter CytoFLEX-LX, Beckman) (Figure S11B).

Article Title: Single-Cell Transcriptomics Uncover EEF1A1-Driven Ubiquitination Dysregulation in T Cell Exhaustion and SLE Pathogenesis via STAT1-Mediated Th1/Th2 Imbalance
Article Snippet: .. For surface staining, 5 μL anti-CD4 (Elabscience, E-AB-F1097C) was added and incubated in the dark at 4°C for 30 min. ..

Article Title: Helminth reshapes host gut microbiota and immunoregulation by deploying an antimicrobial program of innate immunity.
Article Snippet: .. Briefly, the cells were stained with antibodies of Fixable Viability Dye (Cat. 65-0866-14, eBioscience, 1 μL/mL) for dead cells, and antiCD16/32 mAbs (Cat. E-AB-F0997A, eBioscience, 10 μg/mL) to block Fc receptors, followed by staining with antibodies against surface markers, including anti-CD3 (Cat. E-ABF1013J, eBioscience, 50 μL/mL), and anti-CD4 (Cat. E-AB-F1097S, Elabscience, 50 μL/mL). .. For intracellular markers, cells were fixed and permeabilized using a Fixation/Permeabilization kit (Cat.00-5123-43, Invitrogen, 1:3 dilution) and stained for anti-FoxP3 (Cat, E-AB-F1238D, Elabscience, 50 μL/mL) and anti-Helios (Cat. 11-9883-82, eBioscience, 2.5 μg/mL) at 4°C for 1 h. The results were analyzed on a flow cytometer (Coulter CytoFLEX-LX, Beckman) (Figure S11B).

Blocking Assay:

Incubation:

Image Search Results

Effects of systemic treatment with an anti-IL-16 or an anti-CD4 antibody on the hypernociception measured 2 days after sciatic ligation in male and female mice. a General schema of the experimental behavioural procedure. b , c The s.c. administration of an anti-IL-16 antibody 1 h before testing dose-dependently inhibited neuropathic thermal hyperalgesia ( b ; 1–10 µg/kg; n = 5–6) and mechanical allodynia ( c ; 0.01–1 µg/kg; n = 5–7) in male mice. d , e Inhibitory effect evoked in female mice after the s.c. administration of the anti-IL-16 antibody of neuropathic thermal hyperalgesia ( d ; 10 µ/kg; n = 5) and mechanical allodynia ( e ; 1 µg/kg; n = 6) 1 h before testing. f , g The s.c. administration of an anti-CD4 antibody 1 h before testing dose-dependently inhibited neuropathic thermal hyperalgesia ( f ; 1–10 µg/kg; n = 5–7) and mechanical allodynia ( g ; 0.01–0.1 µg/kg; n = 5–6) in male mice. h , i Inhibitory effect evoked in female mice after the s.c. administration of the anti-CD4 antibody of neuropathic thermal hyperalgesia ( h ; 10 µ/kg; n = 5) and mechanical allodynia ( i ; 0.1 µg/kg; n = 6–8) 1 h before testing

Journal: Molecular Neurobiology

Article Title: Neural Expression of IL-16 Mediates Neuropathic Pain after Sciatic Injury in Mice

doi: 10.1007/s12035-026-06280-2

Figure Lengend Snippet: Effects of systemic treatment with an anti-IL-16 or an anti-CD4 antibody on the hypernociception measured 2 days after sciatic ligation in male and female mice. a General schema of the experimental behavioural procedure. b , c The s.c. administration of an anti-IL-16 antibody 1 h before testing dose-dependently inhibited neuropathic thermal hyperalgesia ( b ; 1–10 µg/kg; n = 5–6) and mechanical allodynia ( c ; 0.01–1 µg/kg; n = 5–7) in male mice. d , e Inhibitory effect evoked in female mice after the s.c. administration of the anti-IL-16 antibody of neuropathic thermal hyperalgesia ( d ; 10 µ/kg; n = 5) and mechanical allodynia ( e ; 1 µg/kg; n = 6) 1 h before testing. f , g The s.c. administration of an anti-CD4 antibody 1 h before testing dose-dependently inhibited neuropathic thermal hyperalgesia ( f ; 1–10 µg/kg; n = 5–7) and mechanical allodynia ( g ; 0.01–0.1 µg/kg; n = 5–6) in male mice. h , i Inhibitory effect evoked in female mice after the s.c. administration of the anti-CD4 antibody of neuropathic thermal hyperalgesia ( h ; 10 µ/kg; n = 5) and mechanical allodynia ( i ; 0.1 µg/kg; n = 6–8) 1 h before testing

Article Snippet: Subsequently, samples were incubated overnight at 4 °C in a humidified chamber with either a rabbit polyclonal anti-IL-16 antibody (1:100; Invitrogen PA5-82,627), a rabbit recombinant monoclonal anti-CD4 antibody (1:200; Proteintech 86,300–3-RR).

Techniques: Ligation

Time course of anti-IL-16 and anti-CD4 antibodies on thermal hyperalgesia measured 2 days after sciatic ligation in mice. Effects of systemic administration of an anti-IL-16 or an anti-CD4 antibody on hypernociception measured 9 days after sciatic ligation. a Schema of time course of the study of the antihyperalgesic effects induced by the anti-IL-16 or anti-CD4 antibodies in mice submitted to nerve ligation 2 days before. b , c Withdrawal latencies measured in mice 2 days after nerve ligation by the unilateral hot plate test 0, 1, 2, 4 and 6 h after the s.c. administration of anti-IL16 antibody ( b ; 10 µg/kg; n = 6), an anti-CD4 antibody ( c ; 10 µg/kg; n = 6) or the corresponding IgG2bk isotype ( b , c ; IgG2bk 10 µg/kg; n = 6 in each case). Each point represents the mean and corresponding standard error. • p < 0.05, •• p < 0.01 compared with the measure done at time 0, before drug administration; ** p < 0.01 compared with right paws of mice treated with IgG2bк isotype at the corresponding time, two-way ANOVA followed by Tukey’s test

Journal: Molecular Neurobiology

Article Title: Neural Expression of IL-16 Mediates Neuropathic Pain after Sciatic Injury in Mice

doi: 10.1007/s12035-026-06280-2

Figure Lengend Snippet: Time course of anti-IL-16 and anti-CD4 antibodies on thermal hyperalgesia measured 2 days after sciatic ligation in mice. Effects of systemic administration of an anti-IL-16 or an anti-CD4 antibody on hypernociception measured 9 days after sciatic ligation. a Schema of time course of the study of the antihyperalgesic effects induced by the anti-IL-16 or anti-CD4 antibodies in mice submitted to nerve ligation 2 days before. b , c Withdrawal latencies measured in mice 2 days after nerve ligation by the unilateral hot plate test 0, 1, 2, 4 and 6 h after the s.c. administration of anti-IL16 antibody ( b ; 10 µg/kg; n = 6), an anti-CD4 antibody ( c ; 10 µg/kg; n = 6) or the corresponding IgG2bk isotype ( b , c ; IgG2bk 10 µg/kg; n = 6 in each case). Each point represents the mean and corresponding standard error. • p < 0.05, •• p < 0.01 compared with the measure done at time 0, before drug administration; ** p < 0.01 compared with right paws of mice treated with IgG2bк isotype at the corresponding time, two-way ANOVA followed by Tukey’s test

Techniques: Ligation, Hot Plate Test

Journal: Molecular Neurobiology

Article Title: Neural Expression of IL-16 Mediates Neuropathic Pain after Sciatic Injury in Mice

doi: 10.1007/s12035-026-06280-2

Figure Lengend Snippet: Inhibition of neuropathic hypernociception by i.sc. injection of an anti-CD4 antibody. Expression of CD4 receptors in sciatic nerves and up-regulation after nerve injury. Absence of CD3 labelling in the sciatic injured nerve and lack of effect of lymphocyte depletion on neuropathic thermal hyperalgesia. ( a – c ) Behavioural testing of the effects induced after the intra-sciatic administration of the anti-CD4 antibody in mice submitted to nerve ligation 2 days before. A timeline schema of the procedure is represented in ( a ). The i.sc. administration of an anti-CD4 antibody (50 ng; 1 h before testing) prevents thermal hyperalgesia ( b ; n = 5) and mechanical allodynia ( c ; n = 5) in mice submitted to nerve ligation 2 days before. In ( b and c ), means and their corresponding standard errors are represented, • p < 0.05, •• p < 0.01 compared with mice submitted to sham surgery; ** p < 0.01 compared with values obtained in injured mice treated with IgG2bκ, two-way ANOVA followed by Tukey’s test. ( d ) Representative example of CD4 labelling by immunofluorescence in a nerve coming from a mouse submitted to sham surgery ( d1 ) or nerve ligation ( d2 ) 2 days before. The image in d2 ) corresponds to the proximal side of the ligature closest to DRG. The white arrow indicates the ligation site. ( e ) Percentage of CD4 + immunoreactive surface measured in nerve sections coming from mice submitted to sham surgery or sciatic ligation ( n = 3). Means and their corresponding standard errors are represented, ** p < 0.01 compared with mice submitted to sham surgery, Student’s t test. ( f ) Immunofluorescence image showing a CD4 + cell located in the sciatic nerve compatible with a Schwann cell with its nucleus stained with DAPI, ( g1 – g4 ) CD4 expression in a cross section performed at the first ligation of a sciatic nerve proximal to DRG showing a myelinated axon. Bright field image showing the histological structure compatible with the axon profile and its myelin sheath ( g1 ), DAPI staining (blue, g2 ) and CD4 labelling (green, g3 ) are shown. The merged image ( g4 ) shows a more precise localization of CD4 immunofluorescence. ( h1 – h4 ) CD4 expression in a cross section performed at the first ligation of a sciatic nerve proximal to DRG showing CD4 labelling in a Schwann cell surrounding a myelinated axon. Bright field image without staining shows the histological structure compatible with a Schwann cell surrounding an axon ( h1 ), DAPI staining (blue, h2 ) and CD4 labelling (green, h3 ) are shown. The merged image ( h4 ) shows a more precise localization of CD4 immunofluorescence. ( i ) Representative examples of confocal images of cross sections of injured sciatic nerves labelled with DAPI (blue, i1 ), CD4 (green, i2 ) and the neural marker βIII-tubulin (red, i3 ). The merged image shows the colocalization of CD4 and βIII-tubulin in an axon ( i4 , yellow). ( j ) Representative examples of confocal images of injured sciatic nerves labelled with DAPI (blue, j1 ), CD4 (green, j2 ) and the neural marker βIII-tubulin (red, j3 ). The merged image ( j4 ) shows the labelling of an axon (red) surrounded by a CD4 + cell compatible with the shape of a Schwann cell (green). ( k ) Representative examples of confocal images of injured sciatic nerves labelled with DAPI (blue, k1 ), CD4 (green, k2 ), the Schwann cell marker S100β (red, k3 ). The merged image shows the colocalization of CD4 and S100β + Schwann cell ( k4 , yellow). ( l1 - l4 ) Immunofluorescence images of DAPI (blue) and CD3 (red) labelling in thymus cells ( l1 ) and longitudinal nerve sections coming from mice submitted to nerve ligation 2 days before ( l2 - l4 ). Contrasting with the clear-cut lymphocyte morphology observed in the thymus ( l1 ), no CD3 labelling is observed in nerve ( l2 - l4 ) and the sporadic red labelling signal that appeared in some nerve sections was not associated to DAPI-stained nuclei (Fig. l4 ). ( m - n ) Lack of effect of lymphocyte depletion on the hyperalgesic effect evoked by nerve ligation and on the antihyperalgesic effect evoked by the administration of an anti-IL-16 antibody. m ) Schematic representation of the experimental procedure used to evaluate the functional effect of an anti-IL-16 antibody in lymphocyte-depleted mice submitted to sciatic nerve ligation. n ) Decreased withdrawal latencies are shown in lymphocyte-depleted mice 2 days after nerve ligation. The s.c. administration of the anti-IL-16 antibody (10 µg/kg) reversed this thermal hyperalgesia measured by the unilateral hot plate test 1 h later. Means and their corresponding standard errors are represented, •• p <0.01 compared with the contralateral paw; ** p <0.01 compared with values obtained in injured mice treated with IgG2bκ, two-way ANOVA followed by Tukey’s test.

Techniques: Inhibition, Injection, Expressing, Ligation, Immunofluorescence, Staining, Confocal, Marker, Morphology, Functional Assay, Hot Plate Test, Behavioral Assay

Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 (FOXP3), and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: Research

Article Title: Inverse Vaccine Nanomimics: In situ Antigen-Specific Immune Tolerance Induction for Durable Cardiac Repair Post-Myocardial Infarction

doi: 10.34133/research.1464

Figure Lengend Snippet: Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 (FOXP3), and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: For T cell immunofluorescence labeling, nuclei were labeled with 4′,6-diamidino-2-phenylindole (DAPI) (E-CK-A163, Elabscience, China), CD4 with FITC (E-AB-F1097C, Elabscience, China), and CD127 with Alexa Fluor 555 (16-1271-85, eBioscience, USA).

Techniques: Activation Assay, Immunopeptidomics, Flow Cytometry, Immunofluorescence, Staining, Expressing, Western Blot, Analysis, Phospho-proteomics

Changes in dendritic cell phenotype and regulatory T cell responses in cardiac-draining lymph nodes after myocardial infarction (MI). (A) Representative flow cytometry plots showing CD11c + MHC-II + dendritic cells and programmed death ligand 1 (PD-L1) expression in the Control, Gel@PPM, Gel@PP@Rapa, Gel@OVA-IVNMs, and Gel@IVNMs groups at 7 and 56 d after MI. (B) Quantification of the proportion of PD-L1 + cells within the CD11c + MHC-II + dendritic cell population at 7 and 56 d. (C) Quantification of CD4 + CD25 + FOXP3 + regulatory T cells (Tregs) in lymph node-derived cells from the 5 treatment groups after 48 h of culture under unstimulated Control, OVA, or cardiac lysate antigen (CLA) stimulation at 7 and 56 d. (D) Representative flow cytometry plots of CD25 and Forkhead box P3 (FOXP3) expression within CD4 + T cells in the Gel@OVA-IVNMs and Gel@IVNMs groups following Control, OVA, or CLA stimulation at 7 and 56 d. Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: Research

Article Title: Inverse Vaccine Nanomimics: In situ Antigen-Specific Immune Tolerance Induction for Durable Cardiac Repair Post-Myocardial Infarction

doi: 10.34133/research.1464

Figure Lengend Snippet: Changes in dendritic cell phenotype and regulatory T cell responses in cardiac-draining lymph nodes after myocardial infarction (MI). (A) Representative flow cytometry plots showing CD11c + MHC-II + dendritic cells and programmed death ligand 1 (PD-L1) expression in the Control, Gel@PPM, Gel@PP@Rapa, Gel@OVA-IVNMs, and Gel@IVNMs groups at 7 and 56 d after MI. (B) Quantification of the proportion of PD-L1 + cells within the CD11c + MHC-II + dendritic cell population at 7 and 56 d. (C) Quantification of CD4 + CD25 + FOXP3 + regulatory T cells (Tregs) in lymph node-derived cells from the 5 treatment groups after 48 h of culture under unstimulated Control, OVA, or cardiac lysate antigen (CLA) stimulation at 7 and 56 d. (D) Representative flow cytometry plots of CD25 and Forkhead box P3 (FOXP3) expression within CD4 + T cells in the Gel@OVA-IVNMs and Gel@IVNMs groups following Control, OVA, or CLA stimulation at 7 and 56 d. Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Techniques: Flow Cytometry, Expressing, Control, Derivative Assay

Journal: Research

Article Title: Inverse Vaccine Nanomimics: In situ Antigen-Specific Immune Tolerance Induction for Durable Cardiac Repair Post-Myocardial Infarction

doi: 10.34133/research.1464

Article Snippet: Cells were then surface-stained with fluorophore-conjugated anti-rat CD4 (E-AB-F1105C, Elabscience, China) and CD25 (PE-30314, Finetest, China) antibodies.

Techniques: Activation Assay, Immunopeptidomics, Flow Cytometry, Immunofluorescence, Staining, Expressing, Western Blot, Analysis, Phospho-proteomics

Journal: Research

Article Title: Inverse Vaccine Nanomimics: In situ Antigen-Specific Immune Tolerance Induction for Durable Cardiac Repair Post-Myocardial Infarction

doi: 10.34133/research.1464

Article Snippet: Cells were then surface-stained with fluorophore-conjugated anti-rat CD4 (E-AB-F1105C, Elabscience, China) and CD25 (PE-30314, Finetest, China) antibodies.

Techniques: Flow Cytometry, Expressing, Control, Derivative Assay

Lactate accumulation drives the imbalance between Treg and Th17 cells in HCC (A–D) Representative flow cytometry plots showing the proportion of CD4 + CD25 + FOXP3 + regulatory T (Treg) cells and CD4 + IL-17 + Th17 cells among PBMCs in peripheral blood from healthy controls and HCC patients ( n = 3 per group). The proportion of CD4 + CD25 + FOXP3 + Treg cells increased, while CD4 + IL-17 + Th17 cells decreased in the HCC group compared with controls. (E) Serum lactate concentrations in healthy controls and HCC patients were measured by ELISA kit ( n = 10 per group), showing a significant elevation in the HCC group compared with controls. (F) Quantitative RT-PCR analysis of CD4 + T cells from healthy donors treated with exogenous lactate in vitro revealed increased expression of the Treg marker FOXP3 and decreased expression of the Th17 transcription factor RORγt compared with controls ( n = 3 per group). Data are presented as the mean ± SD. t test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Journal: iScience

Article Title: H3K18 lactylation promotes Treg/Th17 imbalance via PTPRM-STAT3 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2026.117896

Figure Lengend Snippet: Lactate accumulation drives the imbalance between Treg and Th17 cells in HCC (A–D) Representative flow cytometry plots showing the proportion of CD4 + CD25 + FOXP3 + regulatory T (Treg) cells and CD4 + IL-17 + Th17 cells among PBMCs in peripheral blood from healthy controls and HCC patients ( n = 3 per group). The proportion of CD4 + CD25 + FOXP3 + Treg cells increased, while CD4 + IL-17 + Th17 cells decreased in the HCC group compared with controls. (E) Serum lactate concentrations in healthy controls and HCC patients were measured by ELISA kit ( n = 10 per group), showing a significant elevation in the HCC group compared with controls. (F) Quantitative RT-PCR analysis of CD4 + T cells from healthy donors treated with exogenous lactate in vitro revealed increased expression of the Treg marker FOXP3 and decreased expression of the Th17 transcription factor RORγt compared with controls ( n = 3 per group). Data are presented as the mean ± SD. t test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: For Th17 detection, cells were stained with FITC Plus Anti-Human CD4 (FITC-65134, Proteintech) for 30 min in the dark, followed by fixation and permeabilization (00–5523-00, Thermo Fisher Scientific) incubated with IL-17-APC (512333, BioLegend) for 30 min. For Treg analysis, cells were stained with CD4-FITC and CD25-APC (FAB1020A, R&D) for 30 min in the dark, followed by fixation and permeabilization using the same buffer system, and incubated with FOXP3-PE (12–4776-42, Invitrogen) for 30 min. After staining, the cells were washed and resuspended in PBS, and then analyzed using a FACSVerse flow cytometer (BD Biosciences).

Techniques: Flow Cytometry, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Analysis, In Vitro, Expressing, Marker

Journal: iScience

Article Title: H3K18 lactylation promotes Treg/Th17 imbalance via PTPRM-STAT3 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2026.117896

Figure Lengend Snippet: PTPRM as a Potential Target of H3K18 Lactylation and Its Association with Treg/Th17 Balance in HCC (A) Venn diagram showing the overlap between genes with upregulated H3K18la promoter peaks (from CUT&Tag) and genes upregulated at the mRNA level (from RNA-seq) in HCC PBMCs, identifying 21 common candidate genes. (B) CUT&Tag tracks revealing differential H3K18la occupancy at the PTPRM and CCL2 gene loci. HCC samples exhibit increased H3K18la enrichment at the PTPRM locus, while distinct enrichment patterns are observed at the CCL2 locus compared with controls. (C) ChIP-qPCR analysis of H3K18la at the PTPRM locus in primary CD4 + T cells, showing increased occupancy in HCC samples that is reduced by LDHA inhibitor oxamate. (D and E) RT-qPCR analysis of PTPRM (D) and CCL2 (E) mRNA expression in CD4 + T cells isolated from healthy controls and HCC patients. (F and G) Knockdown efficiency of PTPRM in primary human CD4 + T cells transfected with three independent siRNAs or a negative control (si-NC), evaluated by RT-qPCR (F) and western blotting (G). (H) RT-qPCR analysis of FOXP3 mRNA expression in CD4 + T cells following transfection with si-PTPRM, relative to their respective si-NC groups. (I) Flow cytometric analysis of the Treg/Th17 balance after PTPRM knockdown. (J) PTPRM expression profile from the Human Protein Atlas (HPA) database. (K) Single-cell RNA-seq analysis of HCC tumor-infiltrating immune cells ( GSE140228 ). Data are presented as the mean ± SD. t test used for two group, one-way ANOVA used for comparisons among multiple groups, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Techniques: RNA Sequencing, ChIP-qPCR, Analysis, Quantitative RT-PCR, Expressing, Isolation, Knockdown, Transfection, Negative Control, Western Blot, Single Cell

PTPRM regulates Treg/Th17 differentiation through STAT3 dephosphorylation (A and B) Western blot and quantification showing reduced STAT3 Y705 phosphorylation upon PTPRM knockdown, while total STAT3 remained unchanged ( n = 3 per group). (C) RT-qPCR analysis showing that PTPRM knockdown decreased FOXP3 and increased RORγt expression ( n = 3 per group), effects reversed by LLL12 (STAT3 Y705 phosphorylation inhibitor). (D) Representative tumor images from Hepa1-6 syngeneic HCC mice, showing reduced tumor growth after PTPRM silencing. (E) RT-qPCR analysis of PTPRM, FOXP3, and RORγt expression in CD4 + T cells isolated from tumor-infiltrating lymphocytes and spleens of control and sh-PTPRM mice. (F and G) Western blot and quantification of p-STAT3 and total STAT3 in CD4 + T cells from TILs and spleens, showing enhanced STAT3 phosphorylation after PTPRM knockdown. (H) Flow cytometric analysis showing decreased CD4 + CD25 + FOXP3 + Treg cells and increased CD4 + IL-17 + Th17 cells in vivo after PTPRM silencing. (I) Schematic model illustrating that histone lactylation-mediated PTPRM upregulation suppresses STAT3 Y705 phosphorylation, thereby promoting Treg differentiation, inhibiting Th17 polarization, and reshaping the immunosuppressive microenvironment in HCC. Data are presented as the mean ± SD. t test used for two group, one-way ANOVA used for comparisons among multiple groups, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001; ns, not significant.

Journal: iScience

Article Title: H3K18 lactylation promotes Treg/Th17 imbalance via PTPRM-STAT3 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2026.117896

Figure Lengend Snippet: PTPRM regulates Treg/Th17 differentiation through STAT3 dephosphorylation (A and B) Western blot and quantification showing reduced STAT3 Y705 phosphorylation upon PTPRM knockdown, while total STAT3 remained unchanged ( n = 3 per group). (C) RT-qPCR analysis showing that PTPRM knockdown decreased FOXP3 and increased RORγt expression ( n = 3 per group), effects reversed by LLL12 (STAT3 Y705 phosphorylation inhibitor). (D) Representative tumor images from Hepa1-6 syngeneic HCC mice, showing reduced tumor growth after PTPRM silencing. (E) RT-qPCR analysis of PTPRM, FOXP3, and RORγt expression in CD4 + T cells isolated from tumor-infiltrating lymphocytes and spleens of control and sh-PTPRM mice. (F and G) Western blot and quantification of p-STAT3 and total STAT3 in CD4 + T cells from TILs and spleens, showing enhanced STAT3 phosphorylation after PTPRM knockdown. (H) Flow cytometric analysis showing decreased CD4 + CD25 + FOXP3 + Treg cells and increased CD4 + IL-17 + Th17 cells in vivo after PTPRM silencing. (I) Schematic model illustrating that histone lactylation-mediated PTPRM upregulation suppresses STAT3 Y705 phosphorylation, thereby promoting Treg differentiation, inhibiting Th17 polarization, and reshaping the immunosuppressive microenvironment in HCC. Data are presented as the mean ± SD. t test used for two group, one-way ANOVA used for comparisons among multiple groups, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001; ns, not significant.

Techniques: De-Phosphorylation Assay, Western Blot, Phospho-proteomics, Knockdown, Quantitative RT-PCR, Analysis, Expressing, Isolation, Control, In Vivo

Journal: iScience

Article Title: H3K18 lactylation promotes Treg/Th17 imbalance via PTPRM-STAT3 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2026.117896

Figure Lengend Snippet:

Techniques: Isolation

Cytologic, histopathologic, immunohistochemical and flow cytometric findings of the gingival mass and regional lymph nodes. (A) Fine‐needle aspiration cytology of the gingival mass showing a low‐cellularity smear composed of a homogeneous population of round cells. The cells exhibit round to oval, occasionally indented and pleomorphic nuclei, with mild to moderate anisocytosis and anisokaryosis. Some cells contain prominent nucleoli, and occasional multinucleated cells are observed. A single neutrophil is present in the upper right field. (B) Histopathologic examination of the gingival mass demonstrating a densely cellular, poorly demarcated, infiltrative round cell neoplasm with frequent mitotic figures. (C and D) Immunohistochemical staining showing strong and diffuse cytoplasmic immunoreactivity of neoplastic cells for MUM‐1, consistent with extramedullary plasmacytoma. (E) Cytologic evaluation of the submandibular lymph node revealed a predominant population of large, atypical round to ovoid cells with marked nuclear atypia, prominent and multiple nucleoli, binucleation and multinucleation, admixed with small to intermediate‐sized lymphocytes, with one abnormal mitotic figure observed in the field, supporting metastatic involvement of the regional lymph node. (F) Flow cytometric immunophenotyping of the lymph node demonstrating heterogeneous expression of CD5 and CD21, with a predominant population of CD5‐ and CD21‐double‐negative cells, supporting the metastatic involvement of extramedullary plasmacytoma in the regional lymph node. Scale bars: A, E = 10 µm; B, D = 50 µm; C = 200 µm.

Journal: Veterinary Medicine and Science

Article Title: Rare Feline Gingival Extramedullary Plasmacytoma: Clinical Application of Electrochemotherapy for Local Control

doi: 10.1002/vms3.71294

Figure Lengend Snippet: Cytologic, histopathologic, immunohistochemical and flow cytometric findings of the gingival mass and regional lymph nodes. (A) Fine‐needle aspiration cytology of the gingival mass showing a low‐cellularity smear composed of a homogeneous population of round cells. The cells exhibit round to oval, occasionally indented and pleomorphic nuclei, with mild to moderate anisocytosis and anisokaryosis. Some cells contain prominent nucleoli, and occasional multinucleated cells are observed. A single neutrophil is present in the upper right field. (B) Histopathologic examination of the gingival mass demonstrating a densely cellular, poorly demarcated, infiltrative round cell neoplasm with frequent mitotic figures. (C and D) Immunohistochemical staining showing strong and diffuse cytoplasmic immunoreactivity of neoplastic cells for MUM‐1, consistent with extramedullary plasmacytoma. (E) Cytologic evaluation of the submandibular lymph node revealed a predominant population of large, atypical round to ovoid cells with marked nuclear atypia, prominent and multiple nucleoli, binucleation and multinucleation, admixed with small to intermediate‐sized lymphocytes, with one abnormal mitotic figure observed in the field, supporting metastatic involvement of the regional lymph node. (F) Flow cytometric immunophenotyping of the lymph node demonstrating heterogeneous expression of CD5 and CD21, with a predominant population of CD5‐ and CD21‐double‐negative cells, supporting the metastatic involvement of extramedullary plasmacytoma in the regional lymph node. Scale bars: A, E = 10 µm; B, D = 50 µm; C = 200 µm.

Article Snippet: For flow cytometric analysis, antibodies against CD21 (B‐cell marker; clone CA2.1D6, RPE‐conjugated, Bio‐Rad Antibodies, MCA1781R), CD5 (pan–T‐cell marker; clone FE1.1B11, FITC‐conjugated, Bio‐Rad Antibodies, MCA2038F), CD4 (helper T‐cell marker; clone VPG34, FITC‐conjugated; Bio‐Rad Antibodies, MCA1346F) and CD8 (cytotoxic T‐cell marker; clone VPG9, RPE‐conjugated; Bio‐Rad Antibodies, MCA1347R) were used.

Techniques: Immunohistochemical staining, Staining, Expressing

a, Kaplan–Meier survival curves for overall survival (OS) in a published pan-cancer cohort (left) and an immunotherapy cohort (middle), stratified by KRAS mutation and co-mutation subtypes; progression-free survival (PFS) and treatment response in the single-center cohort (right). b, IPS (up) and ESTIMATE score analysis (down) from TCGA (left) and GSE72094 (right) datasets comparing G12D versus non-G12D tumors within STK11-low/co-mutant KL settings. c, Lung weights of Kras^G12D/+;Stk11^f/f (KDL) versus Kras^G12C/+;Stk11^f/f (KCL) mice. d, Single-cell RNA-seq showing proportions of CD8+ T cells, macrophages, and dendritic cells (DCs) in KDL versus KCL tumors. e, f, GSEA of antigen presentation and interferon response pathways in macrophages (e) and DCs (f) from single-cell data. g, Representative IHC images of CD8+ T cell infiltration (left) and quantitative analysis (right) in KL patients with STK11 mutation/low expression versus other subtypes. Data are shown as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: bioRxiv

Article Title: Co-targeting KRAS and BCL-2 induces pyroptosis and antitumor tertiary lymphoid structures

doi: 10.64898/2026.10.12.756217

Figure Lengend Snippet: a, Kaplan–Meier survival curves for overall survival (OS) in a published pan-cancer cohort (left) and an immunotherapy cohort (middle), stratified by KRAS mutation and co-mutation subtypes; progression-free survival (PFS) and treatment response in the single-center cohort (right). b, IPS (up) and ESTIMATE score analysis (down) from TCGA (left) and GSE72094 (right) datasets comparing G12D versus non-G12D tumors within STK11-low/co-mutant KL settings. c, Lung weights of Kras^G12D/+;Stk11^f/f (KDL) versus Kras^G12C/+;Stk11^f/f (KCL) mice. d, Single-cell RNA-seq showing proportions of CD8+ T cells, macrophages, and dendritic cells (DCs) in KDL versus KCL tumors. e, f, GSEA of antigen presentation and interferon response pathways in macrophages (e) and DCs (f) from single-cell data. g, Representative IHC images of CD8+ T cell infiltration (left) and quantitative analysis (right) in KL patients with STK11 mutation/low expression versus other subtypes. Data are shown as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: Mice were injected intraperitoneally with monoclonal antibodies (200 μg/mouse) targeting CD4 (clone GK1.5, BioXCell BE0003-1), CD8 (clone 53-6.7, BioXCell BE0003-1), or NK cells (clone PK136, BioXCell BE0036) twice weekly.

Techniques: Mutagenesis, Analysis, Single Cell, RNA Sequencing, Immunopeptidomics, Expressing

a, b, Antitumor efficacy of combination treatment in KP-1 and FC1242 subcutaneous xenograft models. n = 8 mice per group. c, Lymphoid immune cell composition in KP1 tumors. n = 6 per group. d, Myeloid immune cell composition in KP1 tumors. n = 6 per group. Statistical significance was determined by one-way ANOVA test. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

Journal: bioRxiv

Article Title: Co-targeting KRAS and BCL-2 induces pyroptosis and antitumor tertiary lymphoid structures

doi: 10.64898/2026.10.12.756217

Figure Lengend Snippet: a, b, Antitumor efficacy of combination treatment in KP-1 and FC1242 subcutaneous xenograft models. n = 8 mice per group. c, Lymphoid immune cell composition in KP1 tumors. n = 6 per group. d, Myeloid immune cell composition in KP1 tumors. n = 6 per group. Statistical significance was determined by one-way ANOVA test. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

Techniques: Xenograft Assay, Immune Cell

a, Experimental schematic of the in vivo depletion and adoptive transfer study design. b, Tumor growth curves of mice treated with the combination regimen following depletion of B cells, CD4+ T cells, CD8+ T cells, NK cells, or FcyR blockade. n = 5-8 mice per group. c, Multiplex immunofluorescence staining for C3d, IgG, and CK8/18 on tumor sections from vehicle, single-agent, and combination treatment groups. n = 3 per group. d, Quantification of memory B cells in the spleen and tumor-draining lymph nodes from vehicle and combination treatment groups by flow cytometry. n = 4 per group. e, Quantification of long-lived plasma cells in the bone marrow from vehicle and combination treatment groups by flow cytometry. n = 5 per group. f, Serum levels of tumor-specific antibodies measured by flow cytometry in vehicle and combination treatment groups. n = 3-5 per group. g, (Left) Quantification of plasma cells generated from CD19+ splenocytes stimulated with tumor antigens in vitro. (Right) IgG binding to tumor cells detected by flow cytometry after incubation with culture supernatants from vehicle or combination treatment groups. h, Tumor volume curves of naive recipient mice receiving adoptive transfer of B cells or T cells from vehicle- or combination-treated donor mice, followed by tumor inoculation and half-dose RMC-6236 administration. n = 7 mice per group. i, Rechallenge tumor growth in non-CR and treatment-naive mice. n = 8 mice per group. Statistical significance was determined by one-way ANOVA test. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

Journal: bioRxiv

Article Title: Co-targeting KRAS and BCL-2 induces pyroptosis and antitumor tertiary lymphoid structures

doi: 10.64898/2026.10.12.756217

Figure Lengend Snippet: a, Experimental schematic of the in vivo depletion and adoptive transfer study design. b, Tumor growth curves of mice treated with the combination regimen following depletion of B cells, CD4+ T cells, CD8+ T cells, NK cells, or FcyR blockade. n = 5-8 mice per group. c, Multiplex immunofluorescence staining for C3d, IgG, and CK8/18 on tumor sections from vehicle, single-agent, and combination treatment groups. n = 3 per group. d, Quantification of memory B cells in the spleen and tumor-draining lymph nodes from vehicle and combination treatment groups by flow cytometry. n = 4 per group. e, Quantification of long-lived plasma cells in the bone marrow from vehicle and combination treatment groups by flow cytometry. n = 5 per group. f, Serum levels of tumor-specific antibodies measured by flow cytometry in vehicle and combination treatment groups. n = 3-5 per group. g, (Left) Quantification of plasma cells generated from CD19+ splenocytes stimulated with tumor antigens in vitro. (Right) IgG binding to tumor cells detected by flow cytometry after incubation with culture supernatants from vehicle or combination treatment groups. h, Tumor volume curves of naive recipient mice receiving adoptive transfer of B cells or T cells from vehicle- or combination-treated donor mice, followed by tumor inoculation and half-dose RMC-6236 administration. n = 7 mice per group. i, Rechallenge tumor growth in non-CR and treatment-naive mice. n = 8 mice per group. Statistical significance was determined by one-way ANOVA test. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

Techniques: In Vivo, Adoptive Transfer Assay, Multiplex Assay, Immunofluorescence, Staining, Flow Cytometry, Clinical Proteomics, Generated, In Vitro, Binding Assay, Incubation

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