Is Type 1 Diabetes an Autoimmune Disease or an Immunodeficiency?

The immune system is the guardian of our health, defending our body not only against external aggressions (e.g., viruses, bacteria, parasites), but also against abnormal or cancerous cells. When exposed to different intruders, the immune system develops defences such as antibodies which fight the “invaders” like little soldiers. The immune system usually differentiates between what is part of the body and what is foreign.

However, sometimes the immune system is defective or fails. This might be the result of an autoimmune disease or immunodeficiency. But what is the difference between autoimmune disease and immunodeficiency? Do people living with type 1 diabetes (T1D) have a weakened immune system? Here’s what you need to know.

Type 1 diabetes is an autoimmune disease 

In autoimmune diseases, the immune system misidentifies cells that are part of the body as foreign and dangerous and attacks them. This is the case with T1D, where the immune system identifies the beta cells of the pancreas (insulin-producing cells) as foreign and destroys them. 

Over time, people with T1D lose all their beta cells and can no longer produce insulin. Since insulin is essential to life, people with T1D need to replace this missing hormone by administering insulin several times a day.

The causes of this immune system dysfunction are still largely unknown. However, most experts agree that the onset of T1D is likely triggered by a genetic predisposition and certain environmental factors (e.g., viral infections). Recent studies have observed a very small but measurable increase in the risk of T1D following an infection with COVID-19.

This disruption of the immune system can also lead to the simultaneous development of several autoimmune diseases. It’s not uncommon to see other autoimmune diseases in people with T1D (e.g., celiac disease, thyroid conditions). The immune system of a person with a predisposition can unfortunately fail more than once.

There is currently no cure for T1D, but clinical trials (e.g., VX-880) are being conducted to test stem cell treatments. These treatments consist of replacing destroyed beta cells with healthy beta cells. This way, the pancreas can once again produce insulin to meet the body’s requirements. However, these options involve undergoing an immunosuppressive treatment to reduce the effectiveness of the immune system and prevent it from attacking these new foreign cells.

Type 1 diabetes: is the immune system weakened?

Immune system dysfunction is often referred to as “immune deficiency,” also known as “immunodeficiency” or “immunosuppression.” This happens when the immune system fails, in whole or in part, to fight off foreign agents, which increases vulnerability to infections. Immunodeficiency can be present at birth or occur later in life (e.g., AIDS, immunosuppressive treatments following a transplant, chemotherapy).

People with autoimmune diseases such as type 1 diabetes are not usually considered immunocompromised unless they are taking certain drugs that slow down their immune system (e.g., immunosuppressants).

Even though the immune system of people living with T1D is “dysfunctional,” the body’s ability to defend itself when necessary (e.g., infections) remains unaffected. However, elevated blood sugar levels can reduce the effectiveness of immune defences and feed certain aggressors such as bacteria.

In short, T1D is an autoimmune disease that does not directly involve immunodeficiency.

References :

• Kahaly, George J, and Martin P Hansen. “Type 1 diabetes associated autoimmunity.” Autoimmunity reviews vol. 15,7 (2016): 644-8. doi:10.1016/j.autrev.2016.02.017
• Critchley, Julia A et al. “Glycemic Control and Risk of Infections Among People With Type 1 or Type 2 Diabetes in a Large Primary Care Cohort Study.” Diabetes care vol. 41,10 (2018): 2127-2135. doi:10.2337/dc18-0287
• Carey, Iain M et al. “Risk of Infection in Type 1 and Type 2 Diabetes Compared With the General Population: A Matched Cohort Study.” Diabetes care vol. 41,3 (2018): 513-521. doi:10.2337/dc17-2131