TNIK activates the immune system and stimulates cancer development

TNIK is a newly identified protein that triggers the immune response in healthy T-cells. After an infection with the Epstein-Barr virus, TNIK does not activate the body’s defense mechanisms but instead promotes uncontrolled cell division and thus tumor growth. Scientists at the Helmholtz Zentrum München have published their findings in the renowned specialist journal PLoS Biology.

In a healthy cell, TNIK controls the immune response, cell division and cell death. The newly discovered protein is the central component of a complex that regulates these processes via the NF-κB signaling pathway*. TNIK controls the immune system by activating B cells*. However, if these are infected with the Epstein-Barr virus (EBV)*, the virus takes control of the cells and – also via TNIK – stimulates uncontrolled cell division, which can cause EBV-induced carcinomas and lymphomas. As the research findings show, the team of scientists headed by Dr. Arnd Kieser of the Department of Gene Vectors at the Helmholtz Zentrum München have not only succeeded in explaining a cellular control mechanism, but have also discovered how EBV-dependent tumors are caused.
“Our next step is to look at how we can use TNIK and the TNIK signaling complex as a vantage point to develop new cancer drugs,” says Kieser. The aim of the Helmholtz Zentrum München is to understand the mechanisms that trigger widespread diseases and to deduce new targets for their diagnosis, therapy and prevention.

Further information

Background
* The NF-κB signaling pathway is one of the most under-explored signaling pathways in cells. Amongst other things, it is responsible for controlling cell division, cell death and the immune response.
* The B cells or the B lymphocytes in the immune system.
* The Epstein-Barr virus (EBV) is a widespread human herpes virus that triggers mononucleosis (glandular fever). In immuno-suppressed individuals, EBV often triggers lymphomas and carcinomas.

Original publication:
Shkoda A et al (2012) The Germinal Center Kinase TNIK is Required for Canonical NF-κB and JNK Signaling in B-Cells by the EBV Oncoprotein LMP1 and the CD40 Receptor. PLoS Biol 10(8): e1001376

Specialist contact:
Dr. Arnd Kieser, Helmholtz Zentrum München – German Research Center for Environmental Health, Department of Gene Vectors, Marchioninistrasse 25, 81377 München – Tel.: +49 89-3187-1535 – Fax: +49 89-3187-4225 – E-Mail:

We use cookies to improve your experience on our Website. We need cookies to continually improve our services, enable certain features, and when we embed third-party services or content, such as the Vimeo video player or Twitter feeds. In such cases, information may also be transferred to third parties. By using our website, you agree to the use of cookies. We use different types of cookies. You can personalize your cookie settings here:

Show detail settings
Please find more information in our privacy statement.

There you may also change your settings later.