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Molecular Switch to Enhance the Performance of Immune Cells Identified

Update Date: Jan 21, 2013 08:07 AM EST

In a recent research, scientists were able to find a process which converts CD4 helper T cells into killer T cells. This will enable the immune system to attack the viruses, tumors and other infected cells more aggressively.

In case of a disease, the immune system releases two types of T cells, the CD4 helper and the CD8 killer. The CD8 killer cell is responsible for combating and eliminating the disease-inducing factors. Though it was known that in certain circumstances, the CD4 cells can be converted to CD8 cells, the mechanism was identified in this research.

"We have identified the molecular switch that enables CD4 T cells to override their programming as helper cells and transform into cytolytic (killer) cells. Our team also showed that these transformed helper T cells represent a separate and distinct population of cells. They are not a subset of TH-1 helper cells as previously thought," Hilde Cheroutre, Ph.D., La Jolla Institute scientist and study co-leader, was quoted as saying in MedicalXpress.

"Understanding how these cells derive and what causes them to switch from helper T cells to cytolytic T cells is an important step to learning how to manipulate them in disease, either to turn these cells off in autoimmune disease or turn them on in infectious diseases," Jay A. Berzofsky, M.D., Ph.D., chief of the Vaccine Branch of the National Cancer Institute's Center for Cancer Research, quoted in Medical Xpress.

The work of Dr. Berzofsky in 1980s first identified the ability of a CD4 helper cell to be converted to a CD8 killer cell. Dr. Berzofsky called the recent research a "major advance" and pointed out that the result could be useful in the future of treatment of cancer. "We need all of the cytolytic machinery that we can get to try to destroy cancers. If we can learn to turn them on, I think it's reasonable to believe that these cytolytic T cells can play an important role in controlling cancer," he added.

The research was a joint effort between the La Jolla Institute for Allergy & Immunology and RIKEN Institute in Japan and is published in Nature Immunology.

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