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A new animal study from the Icahn School of Medicine at Mount Sinai has uncovered a mechanism responsible for the development of autoimmune hepatitis. The mechanism, a gene mutation, interferes with the activity of some cells in the immune system and causes them to target the liver.

According to the Mayo Clinic, autoimmune hepatitis occurs when the body's immune system attacks the liver and results in inflammation. Gone untreated, it can lead to cirrhosis and liver failure. Previously, it was unclear what causes the condition, but the Mount Sinai study may have shed some light on the phenomenon.

The researchers sought to explain why T-cells would attack healthy tissues in the body and lead to inflammation and diseases such as rheumatoid arthritis, autoimmune hepatitis and lupus. To find out what causes these reactions, they looked at depleted supplies of medullary thymic epithelial cells (mTECs) in mice. mTECs are supposed to teach T-cells when they should attack tissue, so a lack of them would theoretically cause a number of autoimmune diseases. However, without mTECs, the mice's T-cells went straight for the liver.

"We thought that deleting Traf6 would trigger an autoimmune reaction due to a depletion of mTECs, but did not expect the autoimmune response to be specific to the liver," said Konstantina Alexandropoulos, lead author of the study. "These findings provide an exciting new animal model to study autoimmune hepatitis. We hope that this research will pave the way for new therapies to address a significant unmet need for people with this disease."

Treating autoimmune hepatitis... Full Story

Researchers out of Purdue University have discovered a way to convert blood cells into treatments for autoimmune diseases, such as rheumatoid arthritis and Crohn's disease. By direction the differentiation of T-cells to make them keep autoimmune disease-induced inflammation from developing, scientists can combat some of the painful side effects.

The researchers were able to do this by using naive T-cells - immature cells that all T-cells come from - and turning them into suppressive cells that are able to cease inflammation. The immature cells can be gathered from patients' blood and are altered before getting injected back into the bloodstream.

"These cells are being directed to become a type of cell that is already present in our bodies, where a fine balance between inflammatory T-cells and suppressive T-cells is maintained," said Chang Kim, lead author of the study. "We are just tipping the scales in favor of suppressive T-cells to reduce inflammation."

Kim went on to note that this method of treatment doesn't cause the same side effects that immune-suppressive drugs have, and the fact that the cells are coming from the patients means that the body won't reject them upon injection. He also expressed hope that this treatment strategy be used in patients once every six months, rather than having to take a pill every day.

The report noted that autoimmune diseases are when an individual's immune system attacks his or her body rather than targeting viruses and bacteria. By directing cells to healthy tissue and organs, the immune system actually causes tissue destruction and painful inflammation.

Autoimmune diseases and current treatments... Full Story

Researchers from the Stanford University Medical Center have recently discovered that a gene generally considered to be dead reactivates when inflammation occurs in the body. These findings may shed some light on how anti-inflammatory steroid drugs work, and they have the potential to lead to improved anti-inflammatory treatment.

"Inflammation tells your body something is wrong," said Howard Chang, senior author of the study. "But after it does its job of alerting immune cells to a viral or bacterial infection or spurring them to remove debris from a wound site, it has to get turned off before it causes harm to healthy tissue."

The researchers suspect that this revived gene, known as Lethe, does just that. The report noted that inflammation is a key player in diseases, especially those that are autoimmune-, heart- and neurodegenerative​-related as well as cancer. Traditional treatments, which consist of anti-inflammatory steroids, target the underlying cause of the inflammation.

According to the study, Lethe came back to life, so to speak, after the master regulator of inflammation inside of cells (NF-kappa-B) was activated. The protein kept NF-kappa-B from stimulating the pro-inflammatory genes that cause inflammation. Additionally, the researchers found that Lethe was particularly effective when dexamethasone was used. Dexamethasone is commonly prescribed to fight inflammation, and illicit a response in Lethe that vitamin D, estrogen and male steroid hormones failed to replicate.

"We're wondering whether there might be ways to artificially raise Lethe levels without steroids," said Chang. "These drugs have potentially deleterious side effects such as elevated blood pressure and blood sugar, thinning of bones and general suppression of the immune system."

What does inflammation have to do with autoimmune disease?... Full Story