Scientists at the University of Birmingham are Researching Methods to Reverse Autoimmune Diseases

 

According to an article in Science Alert first published in the journal The Conversation, researchers at the University of Birmingham have shown that it is possible to prevent the immune system’s attack on nerves in autoimmune disorders.

Allergies versus Autoimmune Disorders

Generally, our immune system offers protection from viruses, bacteria, and other pathogens.

In the case of autoimmune disorders such as multiple sclerosis, white blood cells (WBC) do not recognize other cells or tissues as part of the body. They assume that they are foreign invaders and go on the attack.

Researchers at the University of Birmingham are trying to prevent these attacks in autoimmune diseases. They hope to accomplish their goal by exposing the immune system to continually increasing amounts of the molecule that is being attacked by the immune system.

Reversing the Immune System Mode of Attack

Unlike allergic immune disorders, diseases such as multiple sclerosis, type 1 diabetes, and Graves’ disease attack nerves. Thus far, these diseases have been incurable.

The team of researchers explained the mechanism they use to protect patients who have autoimmune diseases. The key is to keep T-cells (a form of WBC) from going on the attack.

T-cells will recognize antigens (or pathogens) and automatically start multiplying as they prepare to attack these invaders. Each T-cell represents parts of molecules produced by antigens.

Immune response genes are turned on to help the T-cells transform from being in a resting mode into an activated state, enabling them to attack pathogens.

After the infection has cleared, a portion of the T-cells become memory T-cells. These T-cells will provide a lifelong immunity by imprinting triggers in chromosomes that enable faster reactivation of rapid immune response genes.

When T-Cells Go Wrong

The myelin sheath is an insulating coating surrounding nerve cells and is unique to the nervous system. In multiple sclerosis, the T-cells misread the myelin basic protein (MBP) which is part of the myelin sheath, reacting to it as if it were an antigen.

The T-cells attack the nervous system, causing multiple sclerosis patients to lose muscle control. In studying this theory, the researchers concentrated on T-cells that misread the MBP.

It was noted over time that the T-cells were gradually less reactive (weakened) after exposure to ever-increasing amounts of the MBP.

They were, in fact, reprogrammed from being an aggressor to being a protector.

The Effect of Reprogramming

Regulating the immune system involves two classes of genes. The first type commands the immune system to attack. The second gene type suppresses the immune system and stops it from losing control.

The team showed that reprogramming the two most important immune suppressor genes caused T-cells to remember to suppress the T-cell receptor. This prevented the T-cells from sending out signals to attack after an encounter with the MBP.

T-cells are responsible for triggering other genes known to activate the immune system but now they were no longer receiving these “attack” signals.

And In The Future . . .

The current treatments for autoimmune disease are far from satisfactory. The treatment usually involves immunosuppressive drugs. These drugs suppress the entire immune system causing the patient to be susceptible to infections and possibly cancer.

The antigen therapy for Graves’ disease and MS is still in the early stages of development. However, short-term results show patients experiencing an improvement in their health during the ongoing clinical trials.

Researchers have confidence in the antigen-based immunotherapy and have expressed hope that their work will lead to cures for all autoimmune diseases.

Rose Duesterwald

Rose Duesterwald

Rose became acquainted with Patient Worthy after her husband was diagnosed with Acute Myeloid Leukemia (AML) six years ago. During this period of partial remission, Rose researched investigational drugs to be prepared in the event of a relapse. Her husband died February 12, 2021 with a rare and unexplained occurrence of liver cancer possibly unrelated to AML.

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