Recently, a paper titled "Canagliflozin impairs T cell effector function via metabolic suppression in autoimmunity" was published online in the international journal Cell Metabolism by scientists from Swansea University and other institutions. They found that canagliflozin may potentially be used to treat autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus, because it can target T cells, which are an essential part of the immune system.

The immune system is a complex network of special cells and organs that protect the body from germs and other foreign invaders. However, when the immune system is overactive, it cannot distinguish between self and non-self and produces autoantibodies by B1 cells that attack and damage its own tissues, resulting in autoimmune diseases. These diseases are characterized by the dysfunction of the affected tissues and organs.

Conventional treatments for autoimmune diseases aim to control the body's excessive immune response and relieve symptoms. Drugs used to treat autoimmune diseases include:

Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Motrin, Advil) and naproxen (Naprosyn).
Disease-modifying anti-rheumatic drugs (DMARDs), such as methotrexate, azathioprine, and sulfasalazine.
Immune-suppressing drugs, such as corticosteroids.

This paper provides a new route—in autoimmunity, T cell function that leads to host damage is often supported by metabolic dysregulation, making immune metabolism a promising target for developing therapies.

Canagliflozin, a type 2 diabetes drug, is a sodium glucose co-transporter 2 (SGLT2) inhibitor with known off-target effects on glutamate dehydrogenase and complex I. However, the effects of SGLT2 inhibitors on human T cell function have not been thoroughly investigated.

The current study suggests that targeting T cell metabolism in autoimmunity may have therapeutic benefits. T cells are a special type of white blood cell that can help fight infection and disease in the body, but in autoimmune diseases, they also attack healthy tissues in the body. They found that canagliflozin can inhibit T cell activation, which may indicate that the drug can be repurposed as a new therapy for T cell-driven autoimmunity.

Dr. Nicholas Jones said: "Our findings are very important because they provide a basis for the clinical development and application of canagliflozin for specific autoimmune diseases. Since the drug is already widely used and has known safety in humans, it may be faster than any new drug to enter clinical trials and bring valuable therapeutic benefits to patients with autoimmune diseases."

Identifying new roles for drugs currently used in other disease contexts is an exciting area of research. Given that this study mainly targets immune cell metabolism, they hope that the potential therapeutic benefits of this study may apply to a broader range of diseases. In the future, they hope that canagliflozin can enter clinical trials to treat specific human autoimmune disorders.


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