- 46-9994-42 - Invitrogen Antibodies PRF1 antibody

Submitted references LINC01123 promotes immune escape by sponging miR-214-3p to regulate B7-H3 in head and neck squamous-cell carcinoma.

Li H, Yang Z, Yang X, Zhang F, Wang J, Wu Z, Wanyan C, Meng Q, Gao W, Yang X, Wei J
Cell death & disease 2022 Feb 3;13(2):109

Human Thymic CD10(+) PD-1(+) Intraepithelial Lymphocyte Precursors Acquire Interleukin-15 Responsiveness at the CD1a(-) CD95(+) CD28(-) CCR7(-) Developmental Stage.

Billiet L, Goetgeluk G, Bonte S, De Munter S, De Cock L, Pille M, Ingels J, Jansen H, Weening K, Van Nieuwerburgh F, Kerre T, Taghon T, Leclercq G, Vandekerckhove B
International journal of molecular sciences 2020 Nov 20;21(22)

NK cells in self-limited HCV infection exhibit a more extensively differentiated, but not memory-like, repertoire.

de Groen RA, Groothuismink ZMA, van Oord G, Kootstra NA, Janssen HLA, Prins M, Schinkel J, Boonstra A
Journal of viral hepatitis 2017 Nov;24(11):917-926

Blocking the recruitment of naive CD4(+) T cells reverses immunosuppression in breast cancer.

Su S, Liao J, Liu J, Huang D, He C, Chen F, Yang L, Wu W, Chen J, Lin L, Zeng Y, Ouyang N, Cui X, Yao H, Su F, Huang JD, Lieberman J, Liu Q, Song E
Cell research 2017 Apr;27(4):461-482

Peritoneal carcinomatosis of colorectal cancer is characterized by structural and functional reorganization of the tumor microenvironment inducing senescence and proliferation arrest in cancer cells.

Seebauer CT, Brunner S, Glockzin G, Piso P, Ruemmele P, Schlitt HJ, Geissler EK, Fichtner-Feigl S, Kesselring R
Oncoimmunology 2016;5(12):e1242543

Immunohistochemical identification of cytotoxic lymphocytes using human perforin monoclonal antibody.

Hameed A, Olsen KJ, Cheng L, Fox WM 3rd, Hruban RH, Podack ER
The American journal of pathology 1992 May;140(5):1025-30

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Intracellular staining of normal human peripheral blood cells with Anti-Human CD56 (NCAM) APC (left) or Anti-Human CD8a APC-eFluor® 780 (Product # 47-0088-42) (right) and Anti-Human Perforin PerCP-eFluor® 710. Cells in the lymphocyte gate were used for analysis.

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 3 Proliferation with IL-15 induces cytotoxic mediators in CD10 + PD-1 + IELps. ( A ) fold expansion of TCRgammadelta + , conventional and IELp cells cultured for 8 days under various conditions (n = 2); ( B ) IFN-gamma, granzyme B and perforin production by unstimulated TCRgammadelta + , conventional and IELp cells incubated for 5 days in the presence of IL-7, IL-15 or IL-15 + IL-12 + IL-18. IFN-gamma, granzyme B, and perforin production measured via intracellular flow cytometry. Bottom: Cytokine production in IELps, plotted for the first and sixth/last generation ( Figure S5 ; mean +- SEM, n = 3); ( C ) flow cytometric analysis of IFN-gamma, granzyme B and perforin production by TCRgammadelta + cells and IELps proliferated for 6 days with IL-15, followed by stimulation with IL-12 + IL-18 for 48 h or with PMA + ionomycin for 4 h (mean +- SEM, n = 3). Dunnett''s multiple comparisons test was used to assess statistically significant differences in cytokine production between the different populations and different interleukins. p -value < 0.05 (*), p < 0.01 (**), and p < 0.001 (***).

Supportive validation

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Experimental details: Fig. 4 Upregulation of LINC01123 or B7-H3 or downregulation of miR-214-3p induces dysfunction of CD8 + T cells. CD8 + T cells were isolated from PBMCs using immunomagnetic beads. After activation and amplification, CD8 + T cells were cocultured with different CAL-27 cell treatment groups. A Expression of TNF-alpha, IFN-gamma, perforin, and granzyme B in CD8 + T-cell population was analyzed with flow cytometry. B Statistical analysis of the results from flow cytometry of CD8 + T cells. C Expression levels of TNF-alpha, IFN-gamma, perforin, and granzyme B in CAL-27-CD8 + T cocultured supernatants, as detected by ELISA. D CCK8 cytotoxicity test of CD8 + T cells. E ELISA was used to assess the immune activity of CD8 + T cells after recombinant human B7-H3 treatment. * P < 0.05 compared with cells without treatment. The experiment was repeated three times.

Supportive validation

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Experimental details: Fig. 6 The function of LINC01123 in HNSCC can be reversed by miR-214-3p silencing. HNSCC cells were transfected with sh-LINC01123 in the presence of inhibitor-NC or miR-214-3p inhibitor. A Relative expression levels of LINC01123, miR-214-3p, and B7-H3 were determined by qRT-PCR. B B7-H3 protein expression was determined by western blot analysis. C CAL-27 cell viability was measured using a CCK8 assay. D Migration of CAL-27 cells was determined by scratch wound-healing assay. E Statistical results of the scratch-healing test. F Migration and invasion of CAL-27 cells, as determined by transwell migration and invasion assay. G Number of migration and invasion cells. H Apoptosis rate and cell-cycle stage were detected by flow cytometry. I Statistical analysis of apoptosis results. J Statistical analysis of cell cycle stage results. K CD8 + T cells were cocultured with CAL-27 cells that had been transfected with plasmids, and the expression of TNF-alpha, IFN-gamma, perforin, and granzyme B in the CD8 + T cells was analyzed by flow cytometry. L Statistical analysis of CD8 + T-cell flow cytometry results. M After different treatments, CAL-27 cells were cocultured with CD8 + T cells, and the expression levels of TNF-alpha, IFN-gamma, perforin, and granzyme B in coculture supernatants were detected by ELISA. N Killing effect of CD8 + T cells on CAL-27 cells, as assessed by CCK8. O Tumor-volume growth curves of the sh-LINC01123 + inhibitor-NC group and sh-LINC01123 + miR-214-3p-inhibit

Supportive validation

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Experimental details: Figure 3 Naive CD4 + T cells are converted to functional Tregs by tumor-infiltrating DCs and tumor conditioned medium (CM). (A-C) Naive CD4 + T cells from peripheral blood of patients with invasive breast carcinoma were co-cultured with or without autologous pDCs isolated from tumor (TI) or peripheral blood (PB) for 9 days in the presence or absence of 30% CM from autologous tumor slices or adjacent normal tissue slices. (A , B) Non-adherent cells from co-cultures were stained for CD3, CD4, CD25 and intracellular Foxp3, and analyzed by flow cytometry. Representative plots of gated CD3 + CD4 + cells (A) and quantification of percentage of Foxp3 + CD25 + cells among CD3 + CD4 + cells (B) are shown (mean +- SEM, n = 19; * P < 0.05, ** P < 0.01, *** P < 0.001 by Student's t -test). (C) Expression of Treg-associated genes, assessed by qRT-PCR normalized to GAPDH , in sorted CD4 + T cells, relative to expression in cultures without DCs or CM (mean +- SEM, n = 19; * P < 0.05, ** P < 0.01, *** P < 0.001 compared with naive CD4 + T cells cultured alone by Student's t -test). (D-G) Effect of naive CD4 + T cell-derived Tregs, obtained by co-culture with TI pDCs and tumor CM as above, on function of autologous tumor-specific CD8 + T cells. Tumor-specific CD8 + T cells were generated for each subject by stimulating autologous PB CD8 + T cells with autologous tumor lysate-pulsed autologous DCs. Tregs were recovered from co-cultures by magnetic sorting. (D) CFSE-labeled CD8 + T ce

46-9994-42

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