Autoimmunity – When the Immune System Attacks Healthy Tissues and Organs
Autoimmunity (AI) comes in many different shapes and sizes. For some, it can be minor and well controlled with minimal effort, but some develop horrible health problems that hugely burden their quality of life. Why do some develop Hashimoto’s disease (autoimmunity of the thyroid gland)? Why do others develop MS or Lupus? The answer is that science does not really know, but likely the answer lies within having a combination of the susceptible genes and environment that triggers them.
Our immune system is charged with protecting our internal physiology from pathogens that exist in the external world. When pathogens such as viruses enter the body, our immune system swoops in to control the situation. Some cells, such as immune cells called B cells, tag the virus for removal so then another type of immune cell called a T cell knows what to attack. Think of it like applying a big red target on the virus’s back. In addition, T cells attack our own infected cells to help prevent the virus from using our cellular machinery to replicate.
Normally, this system works great for keeping us healthy. But unfortunately, sometimes things can go amiss. Rather than attacking pathogens, sometimes our immune system can attack our own healthy cells. This process is known as autoimmunity.
Historically, medicine has viewed autoimmunity as a strictly pathological response. Recent research indicates that some low level of autoimmunity is actually beneficial and present in healthy people.1,2 The theoretical benefits of autoimmunity include a more rapid immune response, maintenance of a healthy cell population, and better cancer prognosis.3
An Immune System Without Control
It’s normal for us to create immune cells that are reactive to our own tissues, it happens every day. 1,2 Fortunately, these cells are destroyed before they can cause too much damage. In autoimmune disease, our quality control system that normally destroys them falters.
As a result, our immune system attacks our tissues and organs causing disease. Common autoimmune diseases include:
- Type 1 diabetes
- Celiac disease
- IBD & Post-infectious IBS
- Systemic lupus erythematosus
- Sjogren syndrome
- Grave’s disease
- Hashimoto’s thyroiditis
- Addison’s disease
- Rheumatoid arthritis
- Multiple sclerosis
What Causes Autoimmunity?
The true cause of pathological autoimmunity is not known. It is clear there is a failure in one or more of the mechanisms that keep autoreactive immune cells from over-proliferating.
Dysfunction in glucocorticoid (stress hormone) signaling may play a role as steroid therapy is often used successfully to control autoimmune disease. Furthermore, stress is known to exacerbate autoimmune disease.4
Another hypothesis put forth by Dr. Alessio Fasano posits that 3 factors are necessary for autoimmune disease. This includes a genetic susceptibility, an environmental trigger, and increased intestinal permeability5 , also known as leaky gut (read more about leaky gut in one of my previous articles here).
Further research is necessary to identify successful approaches to managing autoimmune disease. As a general principle, addressing lifestyle factors that decrease systemic inflammation are important. This includes exercise, diet, stress management and sleep.
If you would like to learn more about the immune system and autoimmunity, we will be discussing all of this and more in our upcoming free webinar on autoimmunity. The webinar is a collaboration with Food Pharmacy and we are privileged to have Lina Nertby Aurell hosting the webinar. To read more about the webinar and to sign up, click here.
This article was originally published as a guest editor post at foodpharmacy.se
By: Graeme Jones, clinical physiologist and CEO at Nordic Clinic Stockholm.
Published: 14/10/2021
References
1. https://www.sciencedirect.com/science/article/abs/pii/S0928468012000818?via%3Dihub
3. https://pubmed.ncbi.nlm.nih.gov/33976418/
4. https://www.sciencedirect.com/science/article/abs/pii/S156899720700170X
5. https://link.springer.com/article/10.1007/s12016-011-8291-x
