Home Living Healthy Aging Well How Immune Cells Facilitate the Spread of Breast Cancer

How Immune Cells Facilitate the Spread of Breast Cancer

Breast Cancer

The human body has its own system in place to fight off diseases and infections. Yes, we are talking about our body’s immune system which acts like soldiers to protect against invaders and dissenters. It seems now that there are loopholes in our body’s immune system which is why some immune cells turns out to be traitors! The findings of a study conducted by Dr. Karin de Visser and her team at the Netherlands Cancer Institute are published in the journal Nature recently. In the study, it was discovered by researchers that certain immune cells are persuaded by breast tumors to facilitate the spread of cancer cells.

Breast cancer is one of those common diseases in women in the Western countries. About one in every eight women is likely to develop breast cancer. Also, it is estimated that of the women who die of this disease, almost 90% die because the cancer has spread to other parts of their body resulting in metastases. One of the focuses of cancer researchers in the recent years has been to understand the process of metastasis. A previous study conducted a couple of years ago had reported that breast cancer patients with a high number of immune cells called neutrophils in their blood are at increased risk of developing metastases. Now, the obvious thing that comes to everyone’s mind is – immune cells are supposed to protect our body. So, why high neutrophil levels are said to worsen outcome in women with breast cancer?

Dr. Karin de Visser, group leader at the Netherlands Cancer Institute, and her team found out that certain type of breast cancer tumor have the ability to create a domino effect of reactions within the immune system. Such tumors send out signals that results in the production of a lot of neutrophils by the immune system. Normally, neutrophils are produced as a part of an anti-inflammatory response. However, the neutrophils produced as a result of signals from tumor behave differently. They have the ability to block the actions of other immune cells, called T cells. T cells are the immune cells that can recognize and kill cancer cells.

The research team also discovered the signaling protein crucial to this process – interleukin 17 also known as IL17. De Visser said that in their experiment, they noticed that IL17 is vital for the increased production of neutrophils. She added that they also found that this is also the molecule that changes the behavior of the neutrophils, causing them to become T cell inhibitory.

Postdoctoral researcher Seth Coffelt, who is also the first author of the paper in Nature showed the importance of the IL17-neutrophil pathway by inhibiting this pathway in a mouse model that mimics human breast cancer metastasis. It was seen that the animals in which these neutrophils were inhibited developed much less metastases than animals from the control group, in which the IL17-neutrophil route was not inhibited. De Visser commented that it is to be noted that the blocking of the IL17-neutrophil route prevented the development of metastases, but did not affect the primary tumor. She is of the opinion that this could be a promising strategy to prevent the tumor from spreading.

Neutrophils have an important role to play in the body – they protect is from infections. So, inhibiting neutrophils altogether seem a bad idea as it would make the patient prone to all kinds of infections. So, inhibition of IL17 definitely sounds like a safer strategy. Anti-IL17 drugs are currently being tested in clinical trials as a treatment for inflammatory diseases, and the good news is that last month the first anti-IL17 based therapy for psoriasis patients was approved by the U.S. Federal Drug Administration. De Visser said that it would be interesting to find out how these drugs respond in breast cancer patients.

References

http://medicalxpress.com/news/2015-03-immune-cells-breast-cancer.html

http://www.sciencedaily.com/releases/2015/03/150330122354.htm