Autoimmune diseases (like arthritis), is a case where your immune system targets your body’s own tissue and destroys it with inflammation, and is understandably extremely interesting to medical scientists.
To put it simply, why would such an otherwise sophisticated and well-constructed body do such a stupid thing?
Scientists from the Technical University of Munich have now explained the process whereby this occurs in detail in a new study in the journal Cell Report.
And this may lead to a clearer path towards a cure for arthritis.
Your immune system must attack and remove everything it considers to be an abnormal biological material. To do this, it uses T-cells to attack invaders, and also to remove cells that have been damaged and that are identified as abnormal.
These T-cells are incredibly strong and often use inflammation to kill invaders.
The only problem? If the cells in your joints, for example, have been slightly damaged by a relatively normal biological process, such as oxidation or by harmless bacteria, these T-cells will destroy your joints until nothing remains of it.
This is where regulatory T-cells, or Tregs, step in. The job of Tregs is to inhibit unnecessarily strong responses by these T-cells and to block unnecessarily strong inflammation.
In other words, when your T cells begin to destroy your joints because your immune system incorrectly labels them as harmful, these Tregs stop the immune overreaction, curb the inflammation, send the T-cells away, thereby saving your joints.
If you have a condition like arthritis, however, then these Tregs are clearly not doing their job, and this is the puzzle that scientists are still trying to solve.
For some reason, particularly in the case of severely inflamed tissue, Tregs lose their identity and stop operating as the brake system that the immune system often needs, particularly in the misinterpreted cases. As such, the authors of the new study used mice to investigate why this happens.
When they observed severely inflamed tissue in mice, they noticed that a protein called Blimp1 was sometimes present and sometimes absent.
When it was present and active, the Tregs worked. When it was absent, the Tregs lost their identity and remained inactive.
When they deliberately removed Blimp1 from the mice’s inflamed tissue, the mice developed something akin to an autoimmune disease.
Not only did the Tregs lose their abilities to inhibit the immune response, but they also seemed to develop properties that made them prone to inflammation promotion.
This is partly why many autoimmune diseases are genetic, as it is a genetic process that activates Blimp1.
This is groundbreaking research, as it is the first time that scientists have managed to get a glimpse of why the immune system is so dysfunctional in autoimmune diseases like arthritis.
Unfortunately, it will still be years before this discovery translates into any form of functional medication for arthritis. Till then, we will have to rely on diet and other lifestyle changes to tackle inflammation.