Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Mar 13;11:245. doi: 10.3389/fimmu.2020.00245

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2020 Bähr, Spielmann, Quandt and Kielstein.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Schematic depiction of the impact of natural killer (NK) cell dysfunction on the increased risk for tumor development in obesity. Dietary factors, like high energy intake or high intake of saturated fatty acids, promote the development of overweight and obesity and mediate direct effects on NK cell function. Obesity is associated with an excessive growth of adipose tissue and a dysregulated secretion of adipokines, like leptin (), adiponectin (), interleukin-6 (), estrogens (), and others. The obesity-related metabolic environment leads to an altered NK cell functionality including a dysbalance of the expression of activating and inhibiting NK cell receptors as well as NK cell receptor ligands (, ) on tumor cells. This NK cell dysfunction is associated with a decreased killing capacity of malignant cells and an increased risk for tumor development.

Inline graphic — Schematic depiction of the impact of natural killer (NK) cell dysfunction on the increased risk for tumor development in obesity. Dietary factors, like high energy intake or high intake of saturated fatty acids, promote the development of overweight and obesity and mediate direct effects on NK cell function. Obesity is associated with an excessive growth of adipose tissue and a dysregulated secretion of adipokines, like leptin (), adiponectin (), interleukin-6 (), estrogens (), and others. The obesity-related metabolic environment leads to an altered NK cell functionality including a dysbalance of the expression of activating and inhibiting NK cell receptors as well as NK cell receptor ligands (, ) on tumor cells. This NK cell dysfunction is associated with a decreased killing capacity of malignant cells and an increased risk for tumor development.

HHS Vulnerability Disclosure