NK Cells Fighting Cancer

Slides:

Advertisements

Similar presentations

Evading Immune Responses and Tumor Immunology

Advertisements

Peer Support: Francesca Peters + Reesha Ranat. A system of biological structures and process that exits to protect against disease Can be divided based.

IMIQUIMOD, AN IMMUNE-RESPONSE MODIFIER, IN THE TREATMENT OF TRANSITIONAL CELL CARCINOMA OF THE BLADDER Douglas Scherr, M.D. Department of Urology New York.

Tumor immunotherapy 张沛张书铭张黎明赵宸赵世刚 Tumour Immunotherapy: questions Can immune stimulators combat cancer? Which forms of immunotherapy can be used?

Cytokines To highlight the major cytokines that are mediators of: (i) natural immunity, (ii) adaptive immunity and (iii) hematopoesis.

Lecture 7 Immunology Cells of adaptive immunity

CELL-MEDIATED IMMUNITY RAHUL KUMAR LOHANA 2K16/MB/50 INSTITUTE OF MICROBIOLOGY UNIVERSITY OF SINDH, JAMSHORO.

Avoiding Immune Detection

Immunotherapy of hepatocellular carcinoma

Heating is a multifunctional adjuvant that affects tumor microenvironment through several intrinsic and extrinsic mechanisms, which could enhance immunotherapy.

Uptake of T-MPs for DC maturation and antigen presentation.

Volume 9, Issue 4, Pages (October 1998)

INTERLEUKIN 10 (IL-10) CATEGORY: RECEPTORS & MOLECULES

Combined A2A receptor and PD-1 blockade is not effective in IFNγ−/− mice. Combined A2A receptor and PD-1 blockade is not effective in IFNγ−/− mice. AT-3ovadim.

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

HER2 mutants V777L, G309A, D769H formed tumors more rapidly than HER2 WT. A, a total of 0.5 × 106 cells of NIH3T3 expressing either HER2 WT or mutant were.

Mechanisms of immune escape in the tumor microenvironment.

Peritumoral injections of poly(I:C) induce type I IFN–dependent cytotoxic immunity and delay the growth of primary and transplanted Hgf-Cdk4R24C melanomas.

Immunology Dr. Refif S. Al-Shawk

2aG4 directly induces monocytic MDSCs to differentiate into dendritic cells and macrophages by binding to phosphatidylserine on their cell surface. 2aG4.

Fig. 5 Extended local release of R848 increases the number of innate and adaptive antitumor immune cells and cytokines. Extended local release of R848.

Anti-CD96 combines with anti–CTLA-4 or anti–PD-1 to suppress experimental and spontaneous lung metastases. Anti-CD96 combines with anti–CTLA-4 or anti–PD-1.

Activity of MAC-321 (i. v. and p. o

IFNα Induces MDSC Maturation and Loss of Suppressive Function

Comparison of conventional NSG and hIL-7 expressing NSG humanized mice

Gene expression signature of NK cells in NSG hL-7xhIL-15 humanized mice. Gene expression signature of NK cells in NSG hL-7xhIL-15 humanized mice. RNA sequencing.

Ablation of PD-L1 in edited T3 sarcoma cells leads to augmented growth inhibition in WT mice. Ablation of PD-L1 in edited T3 sarcoma cells leads to augmented.

Protection from 4T1 tumor rechallenge in treated mice.

Schematic model of the mechanism of Tak1 protection of HSPC survival.

*p<0.05; **p<0.01; ***p<

Mice immunized twice with RRBC showed superior protection to tumor challenge with αGal-positive MC38 colon carcinoma cells compared with mock-immunized.

Effect of HA on hematopoietic recovery in tumor-bearing mice.

PTENP1 sensitizes renal cancer cells to chemotherapy.

Conversion of CD11bhighCD27high NK cells into MDSCs leads to CD11bhighCD27high and CD11bhighCD27low NK cell reduction. Conversion of CD11bhighCD27high.

CD49b+ cells from tumor-bearing mice are more prone to conversion into MDSCs compared with naive CD49b+ cells. CD49b+ cells from tumor-bearing mice are.

coTCRcys-transduced T cells control tumor growth in vivo.

Survival and tumor burden of mice bearing peritoneally disseminated gastric cancer. Survival and tumor burden of mice bearing peritoneally disseminated.

Matriptase-2 inhibited breast tumor development in vivo.

PD-1 inhibition stimulates the proliferation and cytokine secretion of exhausted/senescent CD8+ T cells in vitro. PD-1 inhibition stimulates the proliferation.

OPN mediates maturation from immature DCs to mature DCs

PD-L1 expressed on edited T3 sarcoma cells prevents their immune elimination. PD-L1 expressed on edited T3 sarcoma cells prevents their immune elimination.

Induction of cytotoxic activity in humanized SCC3 tumor-bearing mice treated with anti-PD-1 antibody. Induction of cytotoxic activity in humanized SCC3.

ADU-S100–mediated tumor clearance is dependent on CD4+, CD8+ T cells, and NK cells. ADU-S100–mediated tumor clearance is dependent on CD4+, CD8+ T cells,

5FU-induced specific activation of CD8+ T cells.

N-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. n-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. HEC-1-A.

Antitumor effects of celastrol in vitro and in vivo.

General overview of innate and adaptive immune responses to and regulation of black yeasts. General overview of innate and adaptive immune responses to.

Influenza vaccine enhances NK cell function through IFN-α.

Prostaglandin E2 attenuates the host antitumor immunity to promote the HFD-induced HCC development. Prostaglandin E2 attenuates the host antitumor immunity.

DAC treatment alters immune cell composition and enhances cytokine production in the peritoneal lavage. DAC treatment alters immune cell composition and.

A to C, MetMAb shows strong antitumor activity in the KP4 orthotopic model of pancreatic cancer by ultrasound. A to C, MetMAb shows strong antitumor activity.

C7R enhances adoptive T-cell immunotherapy against metastatic and intracranial malignancies.A and B, 1 × 106 CHLA-255 FFluc cells were injected i.v. into.

Effect of inhibiting HO-1 on adaptive immune- and cytokine-dependent regulation of tumor growth. Effect of inhibiting HO-1 on adaptive immune- and cytokine-dependent.

Tumor protection induced by therapeutic PLG vaccination in combination with blockade antibodies. Tumor protection induced by therapeutic PLG vaccination.

Immunotherapy of NK-92-S3KD increases anticancer effector productions in HepG2-bearing mice. Immunotherapy of NK-92-S3KD increases anticancer effector.

CDV potentiates the antitumor effect of ionizing radiation in mice intracerebrally implanted with human glioblastoma cells. CDV potentiates the antitumor.

TCR stimulation by agonistic mAb in vivo administration inhibits mouse T-ALL development. TCR stimulation by agonistic mAb in vivo administration inhibits.

The CCR5+ population of SUM-159 cells is enriched with tumor-initiating cells. The CCR5+ population of SUM-159 cells is enriched with tumor-initiating.

Effect of MZ treatment on lung colony formation in an experimental metastasis. Effect of MZ treatment on lung colony formation in an experimental metastasis.

Proliferation of TA3-Ha and TA3-St cells in vitro and in vivo.

TGFβ1/Smad3 signaling suppresses IFNγ production via an E4BP4-dependent mechanism in NK-92 cells. TGFβ1/Smad3 signaling suppresses IFNγ production via.

Impact of IFNγ in B16 melanoma metastasis.

BCMab1 confers Fc-FcγR–dependent antitumor activity through both macrophages and NK cells. BCMab1 confers Fc-FcγR–dependent antitumor activity through.

Enhanced antitumor effects with combination IL21 and anti–PD-1/anti–Tim-3 therapy. Enhanced antitumor effects with combination IL21 and anti–PD-1/anti–Tim-3.

Induction of PD-1 in B cells by TLR agonists and primary HCC-SN.

CD8+ depletion and IFN-γ–deficient myeloid cells and lung metastasis inhibition in Tgfbr2MyeKO mice. CD8+ depletion and IFN-γ–deficient myeloid cells and.

Depletion of CD8+, CD4+, and Ly6G+ cells in subcutaneous TUBO tumor-bearing BALB/c mice treated with KM100 + MTX. Depletions were conducted by intraperitoneal.

Knockdown of ROR1 increases the invasive potential of melanoma cells in vitro and in vivo. Knockdown of ROR1 increases the invasive potential of melanoma.

Silencing E4BP4 abrogates the promoting effect of SMAD3 knockdown on IFNγ production in NK-92 cells. Silencing E4BP4 abrogates the promoting effect of.

RIL21 and checkpoint blockade restore IFNγ production in Tim-3+PD-1+ intratumoral NK cells from cancer patients. rIL21 and checkpoint blockade restore.

Presentation transcript:

NK Cells Fighting Cancer Yac-1 Cell NK Cell Immature Dendritic Cell Lysis Mature Dendritic Cell Th1 Cell Perforin Tumor Cell Destruction IFNγ TNFα, Proinflammatory Cytokines NK cells are stimulated by Yac-1 cells due to their lack of MHC I expression. NK cells lyse immature dendritic cells with perforin. Therefore, only mature dendritic cells survive. Mature dendritic cells then promote a Th1 response. Mice were protected from injected carcinomas if they were treated with Yac-1 cells first, meaning NK cells could potentially help fight back against cancer. Adapted from: Morandi, et al. 2012. PLoS One. 7: e39170. ®