Epithelial-derived cancer cells and tumor-residing APCs have higher HLA-E expression but reduced MHC-1a expression. Epithelial-derived cancer cells and.

Slides:

Advertisements

Similar presentations

Glioma-derived soluble factor(s) enhance IL-10 signaling.

Advertisements

Fig. 2. Comparison of the Th1/Th2 ratio and the percentages of Th1 and Th2 cells between normal and allergic individuals. (A) The Th1/Th2 ratio observed.

Baseline tumor biopsies

AF647-RIS is internalized by TAMs in vivo.

Dominant IL-21 expression in TFH cells correlate with B cell pathology in HIV-infected LNs. Dominant IL-21 expression in TFH cells correlate with B cell.

Body weight at harvest (g) Left kidney:body weight ratio (g/kg)

by Venetia Bigley, Laura E. Spence, and Matthew Collin

Omalizumab treatment downregulates dendritic cell FcεRI expression

Volume 21, Issue 13, Pages (December 2017)

Human dendritic cell subset 4 (DC4) correlates to a subset of CD14dim/−CD16++ monocytes Federica Calzetti, BS, Nicola Tamassia, PhD, Alessandra Micheletti,

Volume 153, Issue 5, Pages e2 (November 2017)

Depo-Provera altered the expression of cell surface markers associated with HIV susceptibility. Depo-Provera altered the expression of cell surface markers.

Depletion of T cells, in particular CD8+ T cells, significantly abrogates HEV neogenesis in tumors. Depletion of T cells, in particular CD8+ T cells, significantly.

Treatment of human MCC tumors with intralesional IFNβ is associated with MHC-I upregulation. Treatment of human MCC tumors with intralesional IFNβ is associated.

Increased chemokine content and leukocyte infiltrate in D6-negative tumors. Increased chemokine content and leukocyte infiltrate in D6-negative tumors.

B7-H4 expression correlates with MHC-I expression and improved prognosis in patients with breast cancer. B7-H4 expression correlates with MHC-I expression.

Figure 2 Alemtuzumab-induced changes in the dendritic cell compartment

Tregs and APC subsets in TDLNs of patients with cervical cancer.

Splenic CD169+ macrophages express a unique gene profile.

Postoperative changes in blood monocyte subsets.

PD-1–PD-L1 axis is highly expressed and is not IFNγ-dependent in a subcutaneous murine model of PDA. A, experimental design for establishment of subcutaneous.

Quantification of MHC-I, β2m, and T-cell subsets.

Human cells produce type I and III IFNs upon Af stimulation.

Differential expression of TRM markers by donor- and recipient-derived T cells with time. Differential expression of TRM markers by donor- and recipient-derived.

Macrophage-resident NRP1 mitigates cytokine release and proinflammatory polarization. Macrophage-resident NRP1 mitigates cytokine release and proinflammatory.

Effect of CD4+ Th1 cytokines and HER2-targeted antibodies on MHC class I restoration and HER2369–377-CD8+ T-cell targeting of HER2-expressing cancer cells.

CPI-444 efficacy requires CD8+ T cells and is associated with increased CD73 expression. CPI-444 efficacy requires CD8+ T cells and is associated with.

Exosome-mediated inhibition of T cells is reversible.

Presence of anti-HPV E6/E7 epitope CD8+ T-cell responses in HPV+ OPSCC tumors. Presence of anti-HPV E6/E7 epitope CD8+ T-cell responses in HPV+ OPSCC tumors.

Fig. 4 Reconstitution of MCs in KitW-sh/W-sh mice increases IL-10+ Breg cells and suppresses the CHS response. Reconstitution of MCs in KitW-sh/W-sh mice.

Expression analysis of IGFBP-3 using human whole-genome microarray.

Increased CCL5 expression, infiltration of Treg cells, and apoptosis of CD8+ T cells in human colorectal tissues. Increased CCL5 expression, infiltration.

PD-L1 expression by DC subsets from lesional CTCL and healthy skin.

FAK overexpression in invasive human breast cancer and DCIS

Treatment with R848 and anti-CD200R leads to changes in the composition of intratumor myeloid cells. Treatment with R848 and anti-CD200R leads to changes.

The selective depletion of DTR-expressing FAP+/CD45+ and FAP+/CD45− tumoral cells from bone marrow chimeric mice by the administration of DTX. A, sketch.

CD94/NKG2A expression and presence is higher on tumor-infiltrating immune cells. CD94/NKG2A expression and presence is higher on tumor-infiltrating immune.

CD94/NKG2A+ TILs lack tissue resident CD103 marker.

pDCs from the melanoma environment responded to TLR-L stimulation.

CD8, galectin-3, galectin-9, and the M1/M2 ratio are associated with a longer survival. CD8, galectin-3, galectin-9, and the M1/M2 ratio are associated.

Immune activity and neopeptide load correlate across tumor types.

Melanoma patient monocytes have altered expression of inflammatory and surface markers. Melanoma patient monocytes have altered expression of inflammatory.

Uptake of TEX by DCs in vivo.

Abnormal monocyte distribution and loss of HLA-DR in patients with stage IV melanoma. Abnormal monocyte distribution and loss of HLA-DR in patients with.

Neutralization of CSF1 and Ad5-HRG treatment.

PD-L1 is expressed in breast cancer.

Immunohistochemical staining for FOXO3a of breast cancer tumor tissues

PD-1 and CD103 are coexpressed on CD8+ T cells but demonstrate distinct mechanisms of regulation. PD-1 and CD103 are coexpressed on CD8+ T cells but demonstrate.

CPI-444 enhances T-cell activation in MC38 tumors.

Anti-CD40 activates TAMs and recruits inflammatory monocytes.

Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.

Combination of R848 and anti-CD200R affects activation of tumor-infiltrating myeloid cells. Combination of R848 and anti-CD200R affects activation of tumor-infiltrating.

Ibrutinib decreases ofatumumab-mediated complement-dependent cytotoxicity. Ibrutinib decreases ofatumumab-mediated complement-dependent cytotoxicity. A,

Flow cytometric gating strategy used to identify CD69 surface expression on CD4 (left paired columns) and CD8 (right paired columns) T lymphocytes. Flow.

Immune profiling of patient-derived organotypic tumor spheroids.

IL35 regulation of tumor growth is accompanied by suppression of CD4+ effector T-cell activity and expansion of Tregs. IL35 regulation of tumor growth.

Increased tumorigenic activities of TIM-3–expressing RCC cells.

Moderate-affinity vaccine antigens elicited greatest antitumor response. Moderate-affinity vaccine antigens elicited greatest antitumor response. Wild-type.

IL-9–expressing TH cells are highly enriched in CCR4+/CCR8+ effector memory TH cells. IL-9–expressing THcells are highly enriched in CCR4+/CCR8+effector.

Fig. 5 IL-5–mediated signaling is critical for the development of CD1dintCD5+ Breg precursor cells and IL-10+ Breg cells. IL-5–mediated signaling is critical.

IL2Cx alone or in combination with anti–CTLA-4 increases the CD8/Treg ratio in the tumor. IL2Cx alone or in combination with anti–CTLA-4 increases the.

Cell counts of immune infiltrate and expression of galectin-1 and galectin-3 in the short-, medium-, and long-term survival cohorts. Cell counts of immune.

NUAK1 overexpression correlates with tumor progression, lymph node infiltrates, and reduced overall survival (OS) in human colorectal cancer. NUAK1 overexpression.

CD36 expression in tissue adjacent and distal to the tumor.

Low initial levels of CD4+ Tregs, proliferating CD8+, and Granzyme B+ CD8+ T cells and high posttreatment tumor MHC class II expression predict better.

EC-derived SP cells are targeted by CD30.CAR T cells.

Bezafibrate increases the number of effector CTLs by enhancing their survival capacity and proliferation. Bezafibrate increases the number of effector.

Coincidence and prognostic significance of PD-1+ and CD103+ cells in HGSC. Serial sections from the 490-case TMA were stained with antibodies to CD103.

Varying the MHC-I affinity, TCR affinity or antigen dose alters the phenotype of CD8 T cells ex vivo. Varying the MHC-I affinity, TCR affinity or antigen.

Phenotyping of T cells. Phenotyping of T cells. Circulating lymphocytes from a tumor-naïve C57BL/6 mice (left column) were compared with those from C57BL/6.

Presentation transcript:

Epithelial-derived cancer cells and tumor-residing APCs have higher HLA-E expression but reduced MHC-1a expression. Epithelial-derived cancer cells and tumor-residing APCs have higher HLA-E expression but reduced MHC-1a expression. A, Representative contour plots of EpCAM expression on cells isolated from paired tumor (TUMOR), paratumor (PARA), and PBMC, with EpCAMhigh cells observed only in tumor-derived tissue identified as epithelial cancer cells, whereas EpCAMdim tumor–derived cells as tumorigenic cells and EpCAMdim paratumor–derived cells as normal epithelial cells. B, Representative gating of HLA-E+ population on tumor-derived EpCAMhigh cancer cells (left), tumor-derived EpCAMdim tumorigenic cells (middle), and paratumor-derived EpCAMdim normal epithelial cells (right). The HLA-E expression (C) and MHC-1a expression (D) by MFI on three different populations of EpCAM-expressing populations. N, number of patients = 10 (esophageal cancer, n = 3; gastric cancer, n = 4; and colorectal cancer, n = 3); one-way ANOVA with Tukey post hoc analysis; F-values, degree of freedom: 5.852,9 (left); 4.163,9 (right). E, Correlative expression of HLA-E and MHC-1a by MFI on CD141+ cDC, CD1c+ cDC, pDC, and inflammatory macrophages derived from paired tumor, paratumor, and PBMC. N, number of patients = 22 (esophageal cancer, n = 7; gastric cancer, n = 8; and colorectal cancer, n = 7); correlative analysis of non-parametric Spearman test of r2 = 0.9747, P < 0.01 for CD141+ cDC; r2 = 0.8174, P < 0.05 for CD1c+ cDC; r2 = 0.9764, P < 0.01 for pDC; and r2 = 0.9085, P < 0.01 for inflammatory macrophages. F, HLA-E expression by MFI on DC subsets from paired tumor, paratumor, and PBMC samples in four different cancer types. (N, number of patients with esophageal cancer = 7; gastric cancer n = 8; colorectal cancer n = 7; and kidney cancer n = 5); one-way ANOVA with Tukey post hoc analysis. Horizontal line, median; interval, 95% confidence; connecting lines, samples from the same patients. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant. Data represent with median ± SEM. Megat Abd Hamid et al. Cancer Immunol Res 2019;7:1293-1306 ©2019 by American Association for Cancer Research