Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
Cells of the Innate Immune Response01:28

Cells of the Innate Immune Response

The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
Phagocytes
Phagocytes police the peripheral tissues by removing cellular debris and responding to the invasion of foreign substances or pathogens. Many phagocytes attack and remove microorganisms even before lymphocytes detect them. The human body has two general...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Reversible loss of hematopoietic stem cells transplant potency by chronic Salmonella infection.

Cell reports·2026
Same author

Treatment patterns and adherence to lipid-lowering therapy, LDL-C control, clinical outcomes, and healthcare resource utilization in treated patients with hypercholesterolemia at high cardiovascular risk in Israel: a retrospective database study.

Frontiers in cardiovascular medicine·2026
Same author

B cell Maturation Antigen Targeted Chimeric Antigen Receptor T Cell Therapy for Refractory Systemic Lupus Erythematosus and Systemic Sclerosis.

Arthritis & rheumatology (Hoboken, N.J.)·2026
Same author

RadD from <i>Fusobacterium nucleatum</i> engages NKp46 to promote antitumor cytotoxicity.

eLife·2026
Same author

Identifying Clones in Myelodysplastic Syndromes by Using Single-Cell RNA Sequencing.

Hematological oncology·2026
Same author

Editorial Expression of Concern: Increased NK cell immunity in a transgenic mouse model of NKp46 overexpression.

Scientific reports·2026

Related Experiment Video

Updated: Jun 13, 2026

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Tumor immunoediting by NKp46.

Moran Elboim1, Roi Gazit, Chamutal Gur

  • 1Lautenberg Center for General and Tumor Immunology, Institute for Medical Research Israel Canada, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

Journal of Immunology (Baltimore, Md. : 1950)
|April 21, 2010
PubMed
Summary
This summary is machine-generated.

Natural killer (NK) cells and NKp46 receptors are crucial in tumor surveillance. This study reveals NKp46-dependent tumor editing in mice, where NKp46 interaction with tumor ligands promotes IFN-gamma secretion and controls tumor growth.

More Related Videos

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses
10:13

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses

Published on: May 6, 2019

Enrichment and Characterization of the Tumor Immune and Non-immune Microenvironments in Established Subcutaneous Murine Tumors
08:32

Enrichment and Characterization of the Tumor Immune and Non-immune Microenvironments in Established Subcutaneous Murine Tumors

Published on: June 7, 2018

Related Experiment Videos

Last Updated: Jun 13, 2026

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses
10:13

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses

Published on: May 6, 2019

Enrichment and Characterization of the Tumor Immune and Non-immune Microenvironments in Established Subcutaneous Murine Tumors
08:32

Enrichment and Characterization of the Tumor Immune and Non-immune Microenvironments in Established Subcutaneous Murine Tumors

Published on: June 7, 2018

Area of Science:

  • Immunology
  • Cancer Biology
  • Cellular and Molecular Immunology

Background:

  • Natural killer (NK) cells are critical for identifying and eliminating abnormal cells, including tumor cells.
  • NKp46 is a key activating receptor on NK cells, recognizing various ligands on target cells.
  • The precise role of NKp46 in the in vivo development of carcinogen-induced tumors remains incompletely understood.

Purpose of the Study:

  • To investigate the role of NKp46 in the recognition and development of 3-methylcholanthrene (MCA)-induced fibrosarcomas.
  • To elucidate the mechanism by which NKp46 influences tumor progression in vivo.

Main Methods:

  • Utilized a 3-methylcholanthrene (MCA)-induced fibrosarcoma model in NKp46-deficient mice.
  • Analyzed the expression of NKp46 ligands on tumors derived from wild-type and NKp46-deficient mice.
  • Assessed the impact of NKp46-ligand interactions on cytokine secretion (IFN-gamma) and tumor cell elimination.

Main Results:

  • Tumor formation rates were similar in NKp46-deficient and wild-type mice.
  • Expression of NKp46 ligands was dependent on NKp46, with higher detection in tumors from NKp46-deficient mice.
  • NKp46-ligand interactions led to IFN-gamma secretion but not direct tumor cell elimination.
  • In vivo tumor growth was dependent on NKp46 and IFN-gamma when NKp46 ligands were highly expressed.

Conclusions:

  • NKp46 plays a role in tumor editing, a process distinct from direct elimination.
  • The interaction between NKp46 and its ligands on carcinogen-induced tumors influences the tumor microenvironment via IFN-gamma.
  • This study uncovers a novel NKp46-mediated mechanism regulating tumor growth and progression.