cd31 microbeads kit (Miltenyi Biotec)
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cd31 microbeads kit
Cd31 Microbeads Kit, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 307 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/microbead+kit/CD31+MicroBead+Kit%2C+human/pm42929833-63-21-24
Average 96 stars, based on 307 article reviews
Cd31 Microbeads Kit, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 307 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/microbead+kit/CD31+MicroBead+Kit%2C+human/pm42929833-63-21-24
Average 96 stars, based on 307 article reviews
cd31 microbeads kit - by Bioz Stars,
2026-11
96/100 stars
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other:Article Title: Human iPSC-derived CNS and retinal microvasculature-on-a-chip models recapitulate hallmarks of diabetic microvascular pathology Article Snippet: On day 15 of differentiation, NCSCs were sorted using Article Title: Tumor-Educated-Platelets interact with Breast Cancer-Stem-Cells via P-selectin- PSGL1 and ensure stemness and metastasis through WNT-β-Catenin-VEGF-VEGFR2 intra-cellular signaling: Therapeutic modulation by aspirin Article Snippet: From the Article Title: Bispecific antibodies specific for PD1 and TIM3 Article Snippet: 105 CD4 T cells were then plated in a 96 well plate together with the B cell line (5:1) in presence or absence of blocking anti-PD1 antibodies (either humanized PD-1 0376, nivolumab or pembrolizumab), anti-TIM3 antibodies (either humanized anti-TIM3 0438 or Kyowa-8213) or anti-PD-1/TIM3 bispecific antibody (humanized 0476) at the concentration of 10 μg/ml. Expressing:Article Title: Human iPSC-derived CNS and retinal microvasculature-on-a-chip models recapitulate hallmarks of diabetic microvascular pathology Article Snippet: On day 5, cells were plated on 0.2 % gelatin-coated plates and cultured in StemPro-34 medium (Thermo Fisher, 10639011) supplemented with 100 ng/ml VEGF-A and 100 ng/ml FGF-2 (Peprotech, HZ-1038, 100-18B). .. On day 10, cells were sorted by CD31 expression using a Article Title: An Advanced Humanized Systemic Lupus Erythematosus Model Enables Parallel Profiling of B Cell-Targeted Therapies Article Snippet: .. Briefly, human fetal liver CD34 + cells were isolated using Isolation:Article Title: An Advanced Humanized Systemic Lupus Erythematosus Model Enables Parallel Profiling of B Cell-Targeted Therapies Article Snippet: .. Briefly, human fetal liver CD34 + cells were isolated using Article Title: Chronic intermittent hypoxia drives M1 macrophage polarization in dorsal root ganglia. Article Snippet: .. Bone marrow cells were then labelled with CD115 ( Flow Cytometry:Article Title: An Advanced Humanized Systemic Lupus Erythematosus Model Enables Parallel Profiling of B Cell-Targeted Therapies Article Snippet: .. Briefly, human fetal liver CD34 + cells were isolated using |
![Continuous TGF-β exposure augmented CD25 expression and enabled superior IL-2–driven growth of long-term FOXP3 ± T cell cultures. (A, B) CD4 + T cells were purified from PBMCs and were activated for 3 d with PHA and 1 nM IL-2 in the presence or absence of 10 nM TGF-β to initiate two long-term lines. TGF-β–cultured T cells and control T cells were then passaged every 3 to 7 d in 1 nM IL-2 with or without 10 nM TGF-β respectively for a total of 38 d. Cells were stained with anti-CD3 PerCP-Cy5.5 (HIT3a), anti-CD4 BV421 (OKT4), anti-CD8 AF700 (SK1), anti-CD25 PE (M-A251), and anti-HLA-DR BUV395 (G46-6). Histograms (A) and bar charts (B) show flow cytometric analyses of cell size (forward scatter) together with CD3, CD4, CD25, and HLA-DR expression (n = 2). (C) Nonfractionated PBMCs (left) and purified CD4 + PBMC T cells (right) were activated and maintained as in panel A for a total of 20 d. To assess IL-2 responsiveness in proliferative assays, TGF-β–cultured T cells and control T cells were incubated with 10 pM–1 nM IL-2 (x-axis) with or without TGF-β in flat-bottomed 96-well plates. Cells were pulsed with [ 3 H]thymidine during the last 24 h of a 72-h culture (counts per minute [CPM]). (D) Independently derived T cell lines were initiated by a 3-d stimulation with PHA (rows 1, 2, 3, and 5) or without mitogen (autologous, row 4). T cells were cultured with 1 nM IL-2 in the presence or absence of 10 nM TGF-β (as designated) from day 0 until the day of analysis (day 12, 26, 38, or 47). Cells were stained with anti-FOXP3 clone PCH101 Alexa Fluor 488. (E) A nonfractionated T cell line was initiated as in panel A followed by continuous propagation in IL-2 and TGF-β for 19 d. Cells were gated on CD3 + and stained with the anti-FOXP3 clone 150D Alexa Fluor 488. Lines used in these experiments were CL2 (A, B), CL1 (C), NL1 (D, rows 1 and 2), CL1 (D, row 3), CL4 (D, row 4), CL2 (D, row 5), and P2 (E). * P < 0.05, ** P < 0.01. FMO, fluorescence minus one; FSC-A, forward scatter area; ns, not significant.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_6443/pmc13686443/pmc13686443__vkag274f1.jpg)
![A neutralizing anti-CD4 mAb inhibited autologous MHCII-restricted autoantigen recognition and IL-2–dependent growth of CD4 ± T-APCs. (A–G) Distinct CD4 + purified (A, D–G) and CD8 + purified (B) T-APC lines were initiated by a 3-d stimulation with PHA in the presence of 1 nM IL-2 and 10 nM TGF-β. Cells were passaged every 3 to 7 d in the presence of TGF-β and IL-2 for a total of 22 d (A), 80 d (B), 10 to 15 d (D-E), 78 d (F), 23 d (G, left two panels), or 36 d (G, right two panels). Human T cells (A, B, D–G) (50,000 cells/well, unless designated otherwise) or mouse SJL-PLP.1 T cells (C) (10,000 cells/well) were cultured with 10 pM, 100 pM, or 1 nM IL-2 (x-axis) in the presence or absence of anti-CD4 mAbs (OKT4 or RPA-T4) or isotype controls (MPC-11 or MOPC-21) in the presence or absence of 10 nM TGF-β. mAb concentrations were 20 μg/mL unless designated as 10 μg/mL. Cultures were pulsed with [ 3 H]thymidine during the last 24 h of a 5-d or 6-d culture unless designated otherwise. T-APC lines used in these experiments were CL5 (A, D), P2 (B), murine SJL-PLP.1 (C), CL6 (E, F), or CL7 (G). Two-way analysis of variance with a Tukey’s multiple comparisons test was used to assess significance. *** P < 0.001, and **** P < 0.0001 for comparisons of the designated mean value(s) at the same IL-2 concentration. CPM, counts per minute; ns, not significant.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_6443/pmc13686443/pmc13686443__vkag274f3.jpg)
![T-APC lines presented agonistic self-antigens and elicited polyclonal Tcon responses while seeding new T-APC lines. (A) JL3 Tcons were derived from freshly isolated PBMCs that were activated with Con-A and 1 nM IL-2 for 4 to 5 d. Tcons were passaged in 1 nM IL-2 in cRPMI media every 4 to 7 d for an additional 29 d. JL2.C5 T-APCs were derived in the presence of GM-CSF, IL-4, IL-2, and TGF-β (1 nM each). JL2.C5 cells were propagated in IL-2 and TGF-β for a total of 92 d (total expansion 10 7.4 -fold). Cells were stained with CD3 BV510 (SK7), CD4 BUV496 (SK3), CD8 Spark Blue 574 (SK1), CD25 PE-Fire 700 (MA251), HLA-DR Spark PLUS UV395 (L243), and CD40L PE (24-31). (B) JL2.C5 T-APCs (day 102) and JL3 Tcons (day 41 postactivation) were cultured for 24 h in the presence or absence of the anti-MHCII mAb L243 or the isotype control (10 μg/mL). (C) Similarly, JL2.C5 T-APCs (day 136) were cultured for 24 h in the presence or absence of anti-MHCII L243, anti-CD40L 5C8, or the isotype control (10 μg/mL). (D, E) Shown are the growth curves for the JL2.C5 T-APCs and the JL3 Tcon lines. (F) Designated densities (x-axis) of senescent nonexpanding JL2.C5 T-APCs (day 129) were added to 96-well plates with JL3 Tcons (day 16, 10 5 /well) in LymphoOne and 1 nM IL-2. Cells were passaged into 24-well plates on day 11. JL3 Tcon expansion was enumerated on day 18 with CountBright Absolute Counting Beads. (G) Cultures derived from panel F were expanded to T25 flasks, and after 2 to 4 wk 3 of these 18 cultures exhibited blastogenic T cell outgrowth. The initiation of the JL3 Tcon/JL2.C5 T-APC coculture (F) was designated as day 0 for initiation of the JL3.B1, JL3.C2, and JL3.T1 lines. (H) To assess whether the JL3.C2 T cells exhibited T-APC activity, JL3 Tcons (10 5 /well, day 39 out of activation) were cultured with designated densities (x-axis) of irradiated JL3.C2 T-APCs (5 Gy) for 5 d in the absence of exogenous mitogen or antigen. Cultures were pulsed with [ 3 H]thymidine during the last 48 h of culture. (I) T-APC lines CL2.2G4 and JL2.C6 and JL3 Tcon lines were compared with the nascent JL3.C2 T-APC line (day 32) for CD40L expression. (J) JL3.C2 T-APCs were cultured without exogenous TGF-β through day 58 and then were cultured with or without 1 nM TGF-β for 4 d. Cells were then subjected to a 10-day passage in duplicate cultures with 1 nM IL-2 in the presence or absence of 1 nM TGF-β without and without 10% heat-inactivated FBS, with manual counts on days 1, 3, 5, and 7 to 11. Cultures were supplemented with 1 nM IL-2 on day 5. (K) CD4 + JL3.C2 (day 70), CD8 + P3 T-APCs (day 14), murine BW5147α/β − cells, or SeAx cells were cultured in triplicate in a 2-d proliferative assay ([ 3 H]thymidine pulse during the last 24 h) with 1 nM IL-2 in the presence of designated titrations of heat-inactivated FBS. (B, C, I) Data were assessed with 1-way analysis of variance with Sidak’s or Dunnett’s multiple comparison test, respectively. (F, H, J, K) Data were assessed with a 2-way analysis of variance with Sidak’s multiple comparison test. ** P < 0.01, *** P < 0.001, **** P < 0.0001.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_6443/pmc13686443/pmc13686443__vkag274f5.jpg)
![T-APC coculture with syngeneic polyclonal Tcons caused an initial activation followed by fratricidal collapse. (A–D) The JL3.C2 T-APC line (day 43, 10 4 /well) and JL3 Tcons (day 39 of rest, 10 5 /well) were cultured alone or together in 96-well plates with 1 nM IL-2 (n = 3). On day 5, cells were passaged to a 24-well plate with 1 nM IL-2. On day 9, cells were subjected to flow cytometric analysis of CD3 BV785 (SK7), CD4 BV421 (OKT4), CD8 Alexa Fluor 700 (SK1), CD25 FITC (M-A251), CD28 BV605 (CD28.2), CD74 PE (LN2), CD86 BV650 (FUN-1), CD134 PE-Cy5 (ACT35), and HLA-DR Spark Plus UV395 (L243). (A) Shown are representative dotplots of the Tcon-derived CD4 + JL3.T1 and JL3.C2 T-APC lines, the combination culture (JL3.C2 T-APCs + JL3 Tcons), and Tcons alone. (B) Mean MFI values are shown for CD4, DN, and CD8 gated cells. Statistical analyses were restricted to comparison of “Both” (i.e. JL3.C2/Tcon cocultures) versus Tcons alone to assess coculture-induced changes in the Tcon phenotype. (C) Cell yields (day 9) were assessed with CountBright Absolute Counting Beads to calculate cell/bead ratios. (D) Manual counting was also used to compare cell yields (day 9) relative to input values for T-APCs (10 4 /well) and Tcons (10 5 /well), given that DN and CD8 + single-positive Tcons comprised approximately 40% of cells by day 9. (E) Total cell yields based on manual cell counting were assessed on days 16, 20, and 24. (F) JL3.C2 T-APCs were cultured without TGF-β for 58 d and then split into parallel cultures with and without 1 nM TGF-β for 3 d. Cells were then tested in a 2-d proliferative assay ([ 3 H]thymidine pulse during the last 24 h) in the presence of 1 nM IL-2 at 10 5 /well (200 µL in LymphoOne) in the presence or absence of 10 µg/mL functional grade anti-CD95 IgM mAb (EOS9.1). (G) CD4 + JL3.C2 T-APCs, CD8 + P3 T-APCs, SeAx T cells, and BW5147α/β − T cells tested in a proliferative assay as described in panel F at 50,000 cells/well with designated dilutions of the EOS9.1 mAb. (E) Data were assessed with an unpaired 2-tailed t test. (C–F) Data were assessed with 1-way analysis of variance with a Tukey’s multiple comparisons test. (B, G) Data were assessed with a 2-way analysis of variance with Sidak’s or Tukey’s multiple comparison test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. CPM, counts per minute. Flow cytometric analyses showed that T-APCs activated resting conventional responder T cells, which subsequently acquired a T-APC phenotype. The activated responder T cells then eliminated the original T-APCs and later exhibited mutual killing, ultimately causing collapse of the culture. Additional experiments showed that T-APCs were highly susceptible to FAS-mediated cell death following treatment with an agonistic cross-linking anti-FAS IgM antibody.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_6443/pmc13686443/pmc13686443__vkag274f10.jpg)
