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Scientists learn how cancer tricks immune system - NOV 3023

Scientists learn how cancer tricks immune system
AM By Alison Caldwell
Posted Mon Nov 12, 2012 10:54am AEDT




MAP: Melbourne 3000

Melbourne scientists say they have made a breakthrough in their research into how cancer cells can trick the body's immune system.


AUDIO: Researchers unlock how cancer deceives body (AM)
Researchers working with mice at the Peter MacCallum Cancer Centre say they have discovered a molecule that a cancer cell produces to convince the immune system that it poses no danger

Lead researcher Dr Dan Andrews says natural killer cells roam the body like a security team looking for disease.

They lock onto the surface of the molecule and if they find everything is fine, they move on.


"Cancer cells are capable... of over-expressing these locks on the surface of the system and they fool the natural killer cell into thinking everything is OK and that's how the cancer grows," he said.

Dr Andrews says it is a major step forward, but any application to cancer treatment is still a long way off.


"The next step is to look and see if this interaction is happening in humans," he said.


"All the work that we've done has been performed in mouse models."

There are hopes the finding could eventually lead to the development of new treatments to interrupt the deadly deception.

"It's taken us five years to get to this point and any translational effects that could flow through in the pipeline are at least 20, 25 years downstream from this," he said.


In collaboration with the University of Melbourne, the research has been funded by the National Health and Medical Research Council and by a foundation called Cancer Cure Australia, which helps fund junior researchers.


The research will be published in the scientific journal Nature Immunology.

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How infection triggers autoimmune disease
Last Updated: Sunday, November 11, 2012,14:39 1
Tags: Infection, Autoimmune disease, Rheumatic fever


Washington: Australian scientists have confirmed a ``weak link`` in the immune system – identifying the exact conditions under which an infection can prompt the body to attack itself.

The medical community has long understood that autoimmune diseases such as rheumatic fever, wherein the body creates antibodies that attack the heart, can develop after the body tries to fight off infections.

But little was known about how these kinds of infection-driven autoimmunity occurred or why the body was unable to prevent them.

Tyani Chan and Robert Brink from Sydney``s Garvan Institute of Medical Research studied mice to investigate what could prompt an infection-driven autoimmune attack.

They were focused on the antibody-creating B cells that play a crucial role in the body`s response to disease.

When the body is fending off an infection, B cells can mutate their antibody genes randomly until they produce one that ``sticks`` to the invading antigen.

This process occurs within specialised environments in the lymph system known as ``germinal centres``.

Dr Chan and Associate Professor Brink demonstrated that when antigen is abundant and available throughout the body, rogue autoantibody-generating B cells are deleted and autoimmunity avoided.

But when target antigen is located only in a tissue or organ remote from the germinal centre, B cells capable of reacting against both antigen and ``self`` are able to escape the germinal centre and produce autoantibodies.

"Essentially we``ve shown there``s a big hole in self-tolerance when it comes to cross-reactive autoantibodies that can attack organ-specific targets," Associate Prof Brink said in a statement.

"Our finding explains a lot about how autoimmune conditions that target particular organs such as the heart or nervous system could develop after an infection.

"It also suggests that if you know enough about the disease and the molecular messaging systems involved, it may be possible in future to modulate the germinal centre response,” he added.

The study has been published in the prestigious international journal Immunity.


First Published: Sunday, November 11, 2012, 10:16



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