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The genetic basis for autoimmunity discovered

March 01, 2002

Researchers from the Basque University have discovered the relationship between E2F2 gene and autoimmunity. The Science Faculty team, leaded by Ana Zubiaga has published the results of its researches in the fifteenth issue of the Immunity magazine.

The team began analysing E2F2 gene and its family. This gene family is responsible for the cell proliferation and the aim of the research was to discover how they work. There are 6 genes on this family and experts do not know yet the reason why there are 6, why they are in different organs, how they are expressed in the growing stages, etc.

They started the investigation with the E2F1 gene. After discovering the power of E2F1 in controlling tumours, they proceed with the E2F2. As they are from the same family they expected to reach similar results, but they did not. The research suggestes that E2F2 could be the key of autoimmunity diseases.

Autoimmunity diseases
Autoimmunity diseases are the consequence of the wrong function of our immunity system. Our immunity system is extremely advanced and protects against foreign virus and bacteria. In order to keep up with this function our immunity system is able to distinguish between our own body cells and foreing ones. However, when an autoimmunity defficiency is detected the system is not able to distinguish those cells and the protection system begins to work. Then anticorps are generated against organs and tissues of the body and those organs suffer a significant damage. Some examples of this kind of diseases are arthritis, lupus erythematosus and sclerosis.

Knock Out
The research is based on the Knock out technique. This technique analyses what happens when the gene is deactivated in order to know what is its function.

In this technique it is essential to use mother cells. In these cells the gene to be analysed is deactivated, that is, a mutate mother cell is created. Afterwards this mutate mother cell is introduced in an embrion, whose development also creates a mutate embrion.

Ana Zubiaga and her team deactivate E2F2 gene in mice. As a consecuence in those mice an abnormal proliferation of T Lymphocytes was found and that could be the key of their autoimmunology disease. So the function of E2F2 is to control the proliferation of cells, more exactly, to control autoimmunity.

Now the same research will be carried out in humans. To do that differences will be analysed between E2F2 gene of healthy people and those who have autoimmunological diseases. If such differences are found, they will force this reseach line for the benefit of those who suffer from such diseases.

Elhuyar Fundazioa

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