There are plenty of loose proteins or other macromolecules free floating everywhere. Why wouldn't they be seized and presented to T cell to trigger an immune response? Does each of these molecules have a signature portion? Or do the presenter cells have some sort of friendly molecule database? Would a normal person's immune system ever possibly generate something like Tocilizumab, i.e. an antibody targeting a normal receptor in most cells?

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    $\begingroup$ What research have you done to try to find the answer to this question yourself? You are expected to do this before posting here. Have you searched for "self-tolerance" or similar terms or phrases? $\endgroup$
    – David
    Feb 23, 2020 at 9:32

1 Answer 1


The immune system of human body can keep human health from disease, but for many people, the immune system is the cause of disease. When the autoimmune system is in disorder, healthy cells and tissues will be killed as viruses, which will lead to a variety of immune system diseases.

Recently, scientists in the United States have discovered the genome that causes the disorder of the human immune system, which is equivalent to the "middle manager" of the immune system. This discovery is likely to bring new hope to the treatment of human immune system diseases, which has been published in the latest issue of nature.

Self defense system out of control immune cells "killing each other"

In the human immune system, a kind of immune cell named T cell is responsible for directly contacting and resisting the invading pathogen. Whether these cells can function normally is controlled by "regulatory T cells". Simply put, "regulatory T cells" are like a "double-edged sword", which can not only prevent T cells from attacking human body's own healthy cells indiscriminately, but when its regulation fails, it will cause immune cells to "kill each other" to normal cells, and its consequences usually include inducing type I diabetes, multiple sclerosis, lupus erythematosus and other immune system diseases.

Scientists have previously found that whether "regulatory T cells" can work normally is related to a major regulatory gene called Foxp3. If Foxp3 is dysfunctional, the human body will lack the active "regulatory T cells". But scientists don't know how Foxp3 controls "regulatory T cells.".

Richard young, a biologist at Whitehead Biomedical Research Institute of Massachusetts Institute of technology and Alexander Marson, a doctor of medicine, and other researchers recently discovered 30 genes directly regulated by Foxp3. It is by combining with these specific genes and regulating their activities that Foxp3 can complete the control of "regulatory T cells". If Foxp3 is the "boss" of the immune system, the 30 genes found in this study belong to the "middle manager".

Immune system diseases are related to the damage of "regulating T cells"

Researchers point out that ten years ago, it was found that the "regulatory T cells" in the human body are responsible for directing the immune system to resist foreign invasion, and the question is why the immune system that should protect health attacks its own cells. Now it has been found that there are gene defects in "regulating T cells" in the body with autoimmune disorder.

When "regulating T cells" cannot guarantee the normal operation of the immune system, the immune system begins to attack cells that should not be attacked. When the "regulatory T cells" were destroyed, several organs of mice developed serious immune system diseases. In some common human immune system diseases, such as multiple sclerosis, there is not no such "regulatory T cells", but there will be some dysfunction. In other words, "regulating T cells" failed to play its due role.

What is the problem of "regulating T cells"? "Studies have shown that when the immune system is disrupted, the activity of these genes is lower than normal. It is this reason that makes the activity of "regulatory T cells" decline, leading to its failure to work properly. Three years ago, scientists have found the main gene controlling "regulatory T cells", which is called Foxp3.

The researchers used DNA biochip technology to scan the complete genome of T cells and map the genes regulated by Foxp3. In the process, the researchers identified 702 Foxp3 binding sites. Until the discovery, the researchers admitted, they had no idea how Foxp3, the main regulator, dictated "regulating T cells.".

Anti rejection treatment for organ transplantation

The latest research shows that the "middle managers" of these 30 immune systems are not working properly. Because "regulatory T cells" are controlled by these specific genes, it can be said that most of the immune system diseases such as type I diabetes, lupus erythematosus, multiple sclerosis, rheumatoid arthritis and so on are determined by these genes.

The next step, the researchers say, is to determine how the 30 specific genes "dictate.". It has been found that these genes are closely related to each other and usually work together to control T cells, but the specific mechanism is still unknown. On the other hand, we should look for chemicals that can simulate the regulation function of Foxp3, the main regulator gene, in order to achieve effective therapeutic immunity.

In addition to the treatment of autoimmune diseases, this finding can also be used for anti rejection treatment in organ transplantation. When performing organ transplantation, once the patient's body rejects the transplanted organ, the operation will fail. Therefore, doctors usually use anti rejection drugs to temporarily inhibit or shut down the immune system.

At present, cyclosporine is mainly used to inhibit the immune system. It can inhibit a protein called activated T-cell nuclear factor (NFAT), which can also be controlled by Foxp3. If necessary, the researchers said, the 30 genes can also be used to "target the target", and the effect of inhibiting the immune system is more obvious.


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