The Researcher Identified A New Mechanism To Eliminate Tumors By Using Immune System

The Researcher Identified A New Mechanism To Eliminate Tumors By Using Immune System

Overview

  • Post By : Microbioz India
  • Source: University of Veterinary Medicine Vienna
  • Date: 19 June, 2016

Team of researcher from the University of Veterinary Medicine – Vienna identified type of signaling to trigger our natural defense mechanism against tumors and team of researcher believe that our immune system not only kick of pathogens as well as cancer tumors too.

 

The discovered signaling molecule named STAT1.Generally our body’s natural killer cells activated by chemical messengers named Cytokines to kill and destroy pathogens as well as tumors, In a brief while activating Natural killer cells, cytokines used molecule STAT 1 which enter in the cell and turn on gene required for activation of NK cells.

 Team of researcher found that in the absence of STAT 1 the tumor cells not eliminated properly and the interesting thing is that STAT1's nuclear activity as transcriptional activator is essential for its function.


 


"The activation of other genes is to date the only known and accepted function of STAT1. In order to show the actual role in the activation of NK cells, we genetically removed this function, "said lead author Eva Putz.

 "It will be an exciting challenge to explore this previously unknown function of STAT1 in tumor surveillance. Improving the mobilization of NK cells in cancer patients is an intense area of research to make anti-tumor therapy more effective," concludes Sexl.

Story source: University of Veterinary Medicine – Vienna

Journal References:

Eva Maria Putz, Andrea Majoros, Dagmar Gotthardt, Michaela Prchal-Murphy, Eva Maria Zebedin-Brandl, Daniela Alexandra Fux, Andreas Schlattl, Robert D. Schreiber, Sebastian Carotta, Mathias Müller, Christopher Gerner, Thomas Decker, Veronika Sexl. Novel non-canonical role of STAT1 in Natural Killer cell cytotoxicity. OncoImmunology, 2016; 00 DOI: 10.1080/2162402X.2016.1186314

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