- 14-0419-80 - Invitrogen Antibodies ITGA2B antibody

Submitted references Platelet Toll-Like-Receptor-2 and -4 Mediate Different Immune-Related Responses to Bacterial Ligands.

Niklaus M, Klingler P, Weber K, Koessler A, Kuhn S, Boeck M, Kobsar A, Koessler J
TH open : companion journal to thrombosis and haemostasis 2022 Jul;6(3):e156-e167

Platelet-Derived GARP Induces Peripheral Regulatory T Cells-Potential Impact on T Cell Suppression in Patients with Melanoma-Associated Thrombocytosis.

Zimmer N, Krebs FK, Zimmer S, Mitzel-Rink H, Kumm EJ, Jurk K, Grabbe S, Loquai C, Tuettenberg A
Cancers 2020 Dec 5;12(12)

SARS-CoV-2 Receptors are Expressed on Human Platelets and the Effect of Aspirin on Clinical Outcomes in COVID-19 Patients.

Sahai A, Bhandari R, Koupenova M, Freedman J, Godwin M, McIntyre T, Chung M, Iskandar JP, Kamran H, Aggarwal A, Kalra A, Bartholomew J, McCrae K, Elbadawi A, Svensson L, Kapadia S, Hariri E, Cameron S
Research square 2020 Dec 23;

Mitochondrial DNA in the tumour microenvironment activates neutrophils and is associated with worse outcomes in patients with advanced epithelial ovarian cancer.

Singel KL, Grzankowski KS, Khan ANMNH, Grimm MJ, D'Auria AC, Morrell K, Eng KH, Hylander B, Mayor PC, Emmons TR, Lénárt N, Fekete R, Környei Z, Muthukrishnan U, Gilthorpe JD, Urban CF, Itagaki K, Hauser CJ, Leifer C, Moysich KB, Odunsi K, Dénes Á, Segal BH
British journal of cancer 2019 Jan;120(2):207-217

The role of platelets in mediating a response to human influenza infection.

Koupenova M, Corkrey HA, Vitseva O, Manni G, Pang CJ, Clancy L, Yao C, Rade J, Levy D, Wang JP, Finberg RW, Kurt-Jones EA, Freedman JE
Nature communications 2019 Apr 16;10(1):1780

Hepatocyte mitochondrial DNA drives nonalcoholic steatohepatitis by activation of TLR9.

Garcia-Martinez I, Santoro N, Chen Y, Hoque R, Ouyang X, Caprio S, Shlomchik MJ, Coffman RL, Candia A, Mehal WZ
The Journal of clinical investigation 2016 Mar 1;126(3):859-64

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure A2 Platelets bound to T cells upon activation in coculture. CD4 + CD25 - T cells were cocultured with or without platelets at the ratio of 1:50 and stimulated with 0.5 ug/mL anti-CD3 mAb and 1.0 ug/mL anti-CD28 mAb for 6 days. At day 1 and 6, platelet-T cell conjugates (CD41a + CD4 + double-positive cells) were analyzed via flow cytometry. For assessment of GARP expression, only CD4 + CD41a- cells were included in the analysis (indicated by the pregating on the upper left (UL)). GARP expression was normalized to the untreated (w/o) control. Dot plots show one representative result of five independent experiments. Isotype controls are shown ( n = 5, box and whiskers, medians + min/max, ** p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 3 Ovarian cancer ascites induces rapid platelet activation and aggregation that is partially abrogated by DNase and protease treatments. a - g Ascites were collected from patients with newly diagnosed advanced EOC and 500 g supernatants (ASC) were used. a Floating aggregates were collected from ascites before centrifugation and analysed by H&E. Abundant neutrophils (black box) and a sparse number of tumour cells (black arrow) embedded in fibrin deposits (pink filaments) were identified. b , c CD41 + PMP were measured in ascites supernatants by modified flow cytometry ( n = 2). Variability exists between different patients (B, left) 16.58% and (C, left) 1.16% CD41a + . In parallel, samples were 0.1 um-filtered to remove microparticles as a specificity control ( b , c , right panels). d - g . Platelets were isolated from peripheral blood of healthy donors and murine cardiac puncture. d Donor platelets were exposed to Tyrode's buffer with 1 mM CaCl 2 (negative control) or ascites supernatants ( n = 7) in the presence of 1 mM CaCl 2 for 30 minutes prior to staining for flow cytometry. Representative density plots show increased number of P-selectin + platelets (P11 gate) after exposure to ascites supernatants, which is quantified to the right (**, p < 0.01 ). E) Naive murine platelets were exposed to the same ascites supernatants ( n = 7), resulting in increased P-selectin expression and loss of CD42d from the surface of platelets within 15 minutes. The proportion of platele

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 1 Characterization of human blood from influenza-infected patients. a - d Blood from influenza-infected patients was fixed after intravenous collection and stained as described in Methods. In all cases DNA was assessed by DAPI. a Many platelets appeared similar to those observed in control blood from healthy donors with a size of 2-5 um. b Some platelets from influenza-infected patients had undergone spreading with a distinctive distribution of CD41. c Platelets and platelet microparticles associated with DNA (arrow). d Spread platelets were found surrounding released DNA with distinct DNA content in their center. Of note, blood from influenza-infected patients and controls in ( a - d ) was not permeabilized. Since formaldehyde can cause certain levels of permeabilization as a function of cross-linking positive staining in control samples for H4 and MPO do not necessarily indicate activation. e - g Levels of proteins related to DNA release in the plasma of influenza-infected patients assessed by ELISA. Source data are provided as a Source Data file. e neutrophil elastase, f myeloperoxidase (MPO), and g histone nucleosome core. The graphs represent the average +- SD of healthy donors ( n = 15) and influenza-infected patients ( n = 18); significance for ( e - g ) was assessed by Mann-Whitney U test, star symbol (*) indicates p < 0.0001. h , i To synchronize time of influenza presence as a function of infection and quantify the released DNA, we

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1. Expression of ACE2 and TMPRSS2 in Platelets by Confocal Microscopy. Platelets isolated from venous blood of healthy individuals was stained for 1h with the following antibodies: CD41 (platelet-specific marker), ACE2, TMPRSS2, and DAPI to eliminate any DNA components. Mounted slides were resolved by confocal fluorescent microscopy using a 100x objective lens. Images are representative of n=6 donors for ACE2 and n=3 for TMPRSS2. Each image represents a different donor. The scale bar is noted.

14-0419-80

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