Molecule that causes rheumatoid arthritis discovered

October 26, 2014

Japanese researchers have identified one of the substances that cause rheumatoid arthritis, an unprecedented finding that could eventually lead to a cure for the disease, media reported Friday.

In patients with rheumatoid arthritis, immune cells mistakenly identify molecules in the body as invasive substances and attack them, resulting in an inflammatory condition that causes joint swelling and pain.

But it has remained unknown which molecules are targeted by the immune cells.

Through experiments with mice, scientists from Kyoto University and other institutes detected one of the target molecules, which is involved in intracellular protein synthesis, Xinhua reported citing the Asahi Shimbun.

The team then found that the immune cells adversely reacted to the identified molecule in 17 percent of all human rheumatoid arthritis patients surveyed.

The findings were published in the US scientific journal Science Oct. 17.

Currently, an estimated 700,000 individuals in Japan suffer from rheumatoid arthritis. Although it is possible to suppress symptoms thanks to the advancement of medicines, there is still no fundamental cure.

In advanced rheumatoid arthritis patients, bones and cartilage are destroyed, affecting the functionality of the limbs.

“If we are able to suppress the function of T cells by using the discovered causative substance as a clue, it could lead to the development of a radical treatment,” said team member Yoshinaga Ito, an assistant professor of immunology at Kyoto University.

In healthy individuals, T cells, the “control tower” for immune cells, detect pathogens invading the body to eliminate them. T cells have various types of censors to respond to differing pathogens, and it is believed that hundreds of millions of types of T cells exist in the human body.

Abnormalities in the control of T cells cause immune cells to attack normal body cells, causing rheumatoid arthritis and other adverse conditions.

Source: Taiwan Sun
Published: 25 Oct 2014

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Category: Education, Features

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