It is vital that the body's own immune system does not overreact.If its key players, the helper T cells, get out of control, thiscan lead to autoimmune diseases or allergies. An immune systemoverreaction against infectious agents may even directly damageorgans and tissues. Immune cells called regulatory T cells ("Tregs") ensure that immuneresponses take place in a coordinated manner: They downregulate thedividing activity of helper T cells and reduce their production ofimmune mediators. "This happens through direct contact betweenregulatory cell and helper cell," says Prof. Peter Krammer of DKFZ."But we didn't know yet what this contact actually causes in helpercells." The researchers' hypothesis was that the contact with theTregs affects certain steps in the complex signaling cascade thatleads to the activation of the helper T cells. |
If the T cell receptor, a sensor molecule on the surface of helpercells, senses foreign or damaged protein molecules, this willtrigger a cascade of biochemical activation reactions. At the endof this signaling cascade, genes that are required for an immuneattack will be read in the nucleus of helper cells. Jointly with colleagues from several German research institutes,Peter Krammer, Angelika Schmidt and co-workers have now comparedthe signaling cascades in helper cells with and without contact toTregs. The immunologists found out that a short contact of the twotypes of cells in the culture dish is sufficient to suppress thehelper cells. Following Treg contact, the typical release ofcalcium ions into the plasma of helper cells does not occur.
As aresult, two important transcription factors, NFkappaB and NFAT, dono longer function. They normally activate genes for immunemediators, thus alerting the immune system. "The mode of action of Tregs is of great importance for cancer medicine. Many of our colleagues have shown in various types ofcancer that Tregs can downregulate the immune response againsttumors so that transformed cells escape the immune defense.
Thiscan contribute to the development and spread of cancer. We aretherefore searching for ways to reactivate such suppressed helpercells," said Krammer, explaining the goals of his work. Fordeveloping immune therapies against cancer it is also crucial tounderstand how Tregs work. The researchers are trying to preventthat immune cells which have been painstakingly activated againstcancer in the culture dish are immediately suppressed again byTregs.
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