An Expert Report on Type 1 Diabetes: Etiology, Effects, and the Evolution of Treatment

Part I: The Autoimmune Enigma: Unraveling the Causes of Type 1 Diabetes

Type 1 diabetes (T1D) is a chronic autoimmune condition that fundamentally alters the body’s ability to produce insulin. Unlike the more common Type 2 diabetes, which is often linked to lifestyle factors and insulin resistance, T1D is a disease of misidentification. The immune system, which is normally tasked with fighting off harmful bacteria and viruses, mistakenly launches an attack on the insulin-producing beta cells within the pancreas.¹ This destructive process is progressive and, over time, leads to a significant or complete cessation of insulin production.¹ Insulin is a crucial hormone for regulating blood sugar levels by helping glucose enter cells for energy. Without sufficient insulin, glucose builds up in the bloodstream, leading to hyperglycemia. A key distinction of T1D, which is critical to understanding the disease and dispelling common misconceptions, is that it cannot be prevented or caused by an individual’s diet, activity level, or lifestyle.¹

The Genetic Blueprint: The Role of the HLA Complex and Other Genes

While the precise trigger for the autoimmune attack remains elusive, scientific consensus points to a complex interplay of genetic and environmental factors.¹ The genetic component is particularly strong, with certain genes accounting for approximately 40% to 50% of the familial aggregation of T1D.⁴ The most significant genetic determinants are found within the human leukocyte antigen (HLA) complex. This complex is a group of genes on chromosome 6 that encode proteins involved in immune function.

Specific polymorphisms of HLA Class II genes, particularly those encoding DQ and DR, confer the highest risk for T1D.⁴ The haplotypes most closely associated with elevated risk are DRB1

03:01 (often abbreviated as “DR3”) and DRB104:01 (abbreviated as “DR4”). Individuals who are heterozygous for both these haplotypes have an odds ratio of 16.59 for developing the disease, a risk significantly higher than for homozygotes.⁴ The inheritance pattern of T1D is further underscored by studies of siblings with the high-risk DR3/4-DQ8 genotype; those who share both HLA haplotypes with an affected sibling have a remarkably high risk of developing the disease, providing strong evidence for the role of MHC-linked genes beyond just the HLA-DR and -DQ alleles.⁵ Conversely, certain haplotypes, such as DRB1*15:01 (DR2), offer strong protection against T1D.⁴ Beyond the HLA region, other genes like insulin,

PTPN22, and CTLA4 are also recognized as susceptibility loci, though their individual contributions to risk are less dramatic than the HLA alleles.⁵

Environmental Triggers: The Catalysts of Autoimmunity

The powerful influence of genetics does not tell the whole story. The observation that even in identical twins—who share 100% of their DNA—the concordance rate for T1D is only between 13% and 33% highlights the critical role of non-genetic, or environmental, factors.⁶ This finding suggests that a genetic predisposition acts as a “tinderbox,” creating a susceptible immune system, but an external trigger is still required to ignite the autoimmune process. A crucial observation supporting this view is the rising incidence of T1D over the past two decades.⁴ Since the genetic makeup of the population has not changed in this short timeframe, the increase in diagnoses points directly to the growing importance of environmental influences.

A leading hypothesis for these triggers is viral infection, particularly by enteroviruses.¹ The theory posits that the body’s immune response to a virus may mistakenly attack the beta cells due to a phenomenon called molecular mimicry, where a viral protein is structurally similar to a protein on the beta cell. In a fascinating and counterintuitive finding, a recent Swedish study discovered that living in a rural environment for the first five years of life could increase the risk of developing T1D by 30% to 80% compared to living in an urban setting.³ This observation challenges the common assumption that urban environments are inherently less healthy. This unexpected geographical link provides a deeper understanding of the environmental trigger hypothesis. It suggests that the

type and diversity of exposures are more important than simple exposure itself. One explanation for this is the “hygiene hypothesis,” which suggests that a lack of early exposure to a wide range of microbial agents in a clean environment may lead to a less-developed or misdirected immune system, making it more prone to autoimmune attacks later in life. This reframes the search for environmental causes from a single infectious agent to a complex ecosystem of microbial, viral, and other potential factors, such as diet and changes in the gut microbiome. Indeed, emerging research suggests that the intestinal flora of individuals who progress to clinical T1D differs from that of nonprogressors, potentially contributing to a proinflammatory metabolic state that precedes the disease.⁶ Studies on migrant populations, which show an increased incidence of T1D when people move from low-incidence to high-incidence areas, provide further evidence of the profound influence of environmental conditions on disease etiology.⁶

Part II: The Health Consequences: Acute Crises and Chronic Damage

The consequences of T1D manifest in two primary forms: acute, life-threatening complications that require immediate medical attention, and chronic, long-term damage that results from prolonged hyperglycemia. These complications define the significant health burden of the disease.

Acute Crises: When Blood Sugar Levels Go Awry

A lack of insulin, whether due to undiagnosed T1D or a missed dose in an existing patient, can lead to a severe metabolic crisis known as diabetic ketoacidosis (DKA).⁷ This is a medical emergency that can be fatal if left untreated.⁹ The pathophysiology of DKA is as follows: without enough insulin, the body’s cells cannot absorb glucose for energy. In response, the body begins to break down fat as an alternative fuel source. This process produces acidic compounds called ketones, which build up in the blood.⁸ This dangerously high concentration of ketones leads to blood acidification and severe dehydration, creating a life-threatening situation.⁹

DKA can be the first presenting symptom of T1D, with up to 40% of newly diagnosed patients experiencing it after missing the earlier signs of the disease.⁹ Key symptoms of DKA range from early indicators like extreme thirst and frequent urination to more severe signs such as nausea, vomiting, abdominal pain, shortness of breath, and a distinctive fruity-scented breath.⁸ Another acute and serious complication of insulin therapy is severe hypoglycemia, or low blood sugar, which occurs when a patient’s treatment regimen is not properly balanced with their activity level, food intake, or other physiological changes.¹⁰

The Long Shadow: Chronic Complications of Hyperglycemia

Over time, sustained high blood sugar levels insidiously damage the body’s blood vessels and nerves, leading to a cascade of chronic complications.¹⁰ This damage reduces blood flow and sensation, impacting virtually every organ system. The long-term effects are categorized as either microvascular (affecting small vessels) or macrovascular (affecting large vessels).

Microvascular complications include:

• Diabetic Retinopathy: Damage to the tiny blood vessels in the eyes can cause them to swell, weaken, or become clogged, leading to vision problems and, in severe cases, blindness.⁷
• Diabetic Nephropathy: The kidneys, which are filled with tiny blood vessels that filter waste, are particularly vulnerable. Hyperglycemia causes these vessels to narrow and become clogged, impairing the kidneys’ function. This condition, known as diabetic kidney disease, is the number one cause of kidney failure in the United States.¹¹ Early detection through urine tests for albumin, a protein that leaks from damaged kidneys, is a crucial preventative measure.¹¹
• Diabetic Neuropathy: High blood sugar levels can damage the blood vessels that supply oxygen to nerves, leading to a loss of sensation, especially in the feet.¹¹ This can mask injuries and infections, which, when combined with poor circulation, can lead to chronic foot ulcers and ultimately amputation.¹²

A particularly insidious causal loop becomes apparent in the progression of these complications. For instance, the onset of kidney disease does not merely add another health problem; it accelerates the progression of others. Damaged kidneys can cause a mineral and bone disorder, where calcium leaches from the bones and deposits in the heart and blood vessels, further contributing to heart disease.¹¹ This demonstrates a dangerous feedback loop where one complication can exacerbate others, emphasizing the central importance of early and aggressive kidney protection as a strategy for preventing a wider range of severe long-term complications.

Macrovascular complications affect the larger blood vessels, increasing the risk of cardiovascular events. High blood sugar promotes the buildup of fatty deposits in the vessels that supply the heart and brain. These deposits can rupture and form blood clots, leading to a heart attack or stroke.¹¹ The significant risk is highlighted by the somber statistic that two out of three people with diabetes die from heart disease or stroke.¹¹ Other chronic issues can include Charcot foot, gum disease, and various sexual and joint problems.¹⁰

Part III: The Evolution of Treatment and Modern Management

The history of T1D treatment is a story of a monumental shift from a fatal diagnosis to a manageable chronic condition, largely thanks to the discovery of insulin and the subsequent advancements in technology.

From Death Sentence to Lifelong Management: The Discovery of Insulin

Before 1921, a diagnosis of T1D was a death sentence, with patients, particularly children, rarely surviving for more than a few years.¹³ The only recourse was a strict, low-carbohydrate diet that could, at best, prolong life for a short time but often led to death by starvation.¹³ This grim reality changed with the groundbreaking work of a young surgeon, Frederick Banting, and his assistant, Charles Best, at the University of Toronto. In 1921, they successfully isolated a pancreatic extract that could reverse diabetes symptoms in dogs.¹³

Working with biochemist J.B. Collip, they purified the extract from the pancreases of cattle, making it safe for human use. In January 1922, 14-year-old Leonard Thompson became the first person to receive an insulin injection.¹⁴ Within 24 hours, his dangerously high blood sugar levels dropped to near-normal. This discovery, which earned Banting and his colleague John Macleod the Nobel Prize in 1923, marked one of the most significant medical breakthroughs in history.¹³ To ensure the treatment was widely accessible, Banting, Best, and Collip sold the patent for the equivalent of one dollar each, a remarkable act of altruism.¹³ The evolution of insulin continued from these crude animal extracts, which often caused allergic reactions, to the first genetically engineered human insulin (Humulin) in 1978 and, later, to a variety of modern, fast- and long-acting insulin analogs that more closely mimic the body’s natural insulin response.¹⁴

The following table summarizes key milestones in this evolution:

Table 1: Key Milestones in Diabetes Treatment

Year	Milestone	Description
1889	Pancreas research	Joseph von Mering and Oskar Minkowski discover a link between the pancreas and diabetes. 14
1910	“Insulin” is named	Sir Edward Albert Sharpey-Shafer proposes that a chemical from the pancreas, which he calls insulin, is missing in people with diabetes. 14
1921	Insulin discovery	Frederick Banting and Charles Best successfully isolate insulin from a dog’s pancreas. 13
1922	First human injection	Leonard Thompson, a 14-year-old, receives the first insulin injection, which saves his life. 13
1978	First human insulin	Scientists create the first genetically engineered human insulin, Humulin, with a structure identical to natural insulin. 14
1986	Insulin pens introduced	Prefilled, convenient pens for insulin injection become available. 17
1990s	Insulin pumps	External insulin pumps are invented, offering continuous insulin delivery. 17
1996	Rapid-acting insulin	The first rapid-acting insulin, Lispro, is introduced, with a faster onset and shorter duration. 16
2017	Ultra-rapid-acting insulin	The first ultra-rapid-acting insulin, Fiasp, is approved, with an even faster onset of action. 16
2023	Teplizumab (Tzield)	The first immunotherapy drug is approved to delay the onset of T1D. 19

The Modern Insulin Arsenal: Types and Delivery Methods

Modern insulin therapy is a complex, tailored approach using a variety of insulin types to mimic the body’s natural response. Insulin is classified by its action profile, including how quickly it begins to work (onset), when it has its maximum effect (peak), and how long its effects last (duration).¹⁸

Insulin Type	Onset	Peak	Duration
Rapid-acting	Within 15 minutes	60 minutes	About 4 hours
Short-acting	30 minutes	90 to 120 minutes	4 to 6 hours
Intermediate-acting	1 to 3 hours	6 to 8 hours	12 to 24 hours
Long- and ultra-long-acting	1 to 6 hours	No distinct peak	14 to 40+ hours

A combination of long-acting and rapid-acting insulin is often used to provide a constant “basal” level of insulin throughout the day and night, with “bolus” doses given before meals to cover carbohydrate intake.²⁰

Insulin cannot be taken orally because stomach enzymes would break it down.²⁰ Therefore, it is administered either through injections—using a fine needle and syringe or a more convenient insulin pen—or via a continuous insulin pump.¹⁸

Empowering Patients: From Finger-Pricks to Continuous Monitoring

The evolution of monitoring technology has been a major advancement in patient care. The move from home blood glucose meters, which require a painful finger-prick to measure blood sugar at a single point in time, to continuous glucose monitors (CGMs) has been transformative.²¹ CGMs use a small sensor inserted under the skin to measure glucose levels every few minutes, providing real-time data and a much more detailed picture of glucose trends throughout the day and night.²² This allows patients and their healthcare teams to identify patterns, make informed decisions, and proactively prevent episodes of hypo- and hyperglycemia.²³

The Artificial Pancreas: The Future Is Now

The most significant recent paradigm shift in T1D management is the development of Automated Insulin Delivery (AID) systems, also known as hybrid closed-loop systems.²⁴ These systems represent a move from reactive to proactive care. An AID system consists of three main components that work in synergy: an insulin pump, a CGM, and a smart algorithm that links the two devices.²⁴ The CGM continuously tracks blood sugar levels and sends the data to the algorithm. The algorithm then uses this real-time and historical data to predict glucose trends and automatically adjust insulin delivery from the pump.²⁴ The system can increase insulin if glucose levels are trending high or even stop delivery to prevent hypoglycemia. This technology reduces the constant, mental burden of managing blood sugar. The profound impact on quality of life and improved clinical outcomes—including better “Time in Range” and fewer hypoglycemic events—has led the American Diabetes Association to call AID systems the new standard of care for T1D.²³

Beyond Medication: The Role of Lifestyle in Management

While technology and insulin are the cornerstones of T1D treatment, a comprehensive management plan is incomplete without attention to lifestyle factors.¹⁸ A fundamental aspect of this is carbohydrate counting, which involves calculating the grams of carbohydrates in a meal and matching the dose of rapid-acting insulin to that count.²⁵ This requires a partnership between the patient and a certified diabetes care and education specialist.

Regular physical activity is also a critical component of care. The American Diabetes Association recommends at least 150 minutes of moderate-to-vigorous aerobic activity per week, along with two to three sessions of resistance exercises.²⁶ However, exercise can significantly impact blood sugar levels, and T1D patients must take precautions. This includes checking blood sugar before, during, and after exercise, having fast-acting carbohydrates available to treat potential hypoglycemia, and, with the guidance of a healthcare professional, adjusting insulin doses as needed.²⁷ A collaborative relationship between the patient and their healthcare team, often facilitated by diabetes self-management education and support (DSMES), is essential for navigating these complexities and optimizing care.²⁵

Part IV: On the Horizon: The Search for a Cure

Current T1D treatments are lifesaving and life-changing, but they are not a cure. The ultimate goal of research is to halt the autoimmune attack and restore the body’s ability to produce its own insulin. This research is converging on two primary strategies: immunotherapy and cell replacement therapy.

Targeting the Root Cause: Immunotherapy

Immunotherapies are new treatments designed to “reprogram” the immune system so that it no longer attacks and destroys the beta cells.³⁰ This is a major philosophical shift from merely replacing insulin to addressing the root cause of the disease. The first significant breakthrough in this area is the drug teplizumab (brand name Tzield), which was approved by the FDA in 2023.¹⁹ Teplizumab is an immunotherapy that can delay the onset of clinical T1D by about two years in people in the preclinical Stage 2 of the disease.¹⁹ It works by slowing the immune system’s attack, providing a “pause button” that can preserve some beta-cell function and make future disease management easier.

A key challenge with immunotherapy is achieving “targeted tolerance” without broad immunosuppression, which carries risks of infection and other side effects.³¹ In a remarkable development from cancer research, scientists at the Mayo Clinic have identified an enzyme,

ST8Sia6, that can “sugar-coat” beta cells with a molecule called sialic acid. This protective coating makes the beta cells appear “normal” to the immune system, effectively hiding them from autoimmune attack.³¹ In lab models, this approach was 90% effective at preventing the onset of T1D, and crucially, it achieved this specific protection without compromising the rest of the immune system’s function.³¹

Cell Replacement and Regeneration

Cell replacement therapy aims to restore insulin production by replacing the destroyed beta cells. Traditional islet cell transplantation involves isolating insulin-producing islets from a cadaver donor’s pancreas and infusing them into a recipient’s liver.³³ This procedure can temporarily reverse diabetes, but its major limitation is the need for patients to take lifelong, systemic immunosuppressive drugs to prevent transplant rejection.³² These drugs carry significant side effects and reduce a patient’s quality of life.³²

A new frontier in this field is stem cell-derived therapy. Vertex Pharmaceuticals’ investigational therapy, VX-880, creates functional, differentiated pancreatic islet cells from stem cells.³⁴ In a Phase 1/2 clinical trial, the first patient treated with VX-880 experienced a robust restoration of islet cell function, with significant increases in C-peptide and improvements in glycemic control.³⁴ This led to a substantial decrease in the need for exogenous insulin and was hailed as an unprecedented result.³⁴

The path to a functional cure will likely involve a synergy of these two research directions. For a cell replacement therapy to be truly curative, the new beta cells must be protected from the very same autoimmune attack that destroyed the original ones. Therefore, immunotherapies that can achieve targeted tolerance or innovative strategies that surface-engineer the new cells to evade immune detection are not just distinct treatments but are necessary complements to cell replacement therapies.³² This combined approach—replacing the destroyed cells while simultaneously preventing a renewed immune attack—is the most promising route to a future where T1D can be fully cured.

Part V: Conclusion

The journey of T1D from a swift, fatal diagnosis to a manageable chronic condition is one of the great medical narratives of the last century. The discovery of insulin by Banting and Best laid the foundation for modern treatment, saving millions of lives and transforming the prognosis for a disease that was once a death sentence. Today, patients benefit from a sophisticated arsenal of insulins, delivery methods, and advanced technologies, with automated insulin delivery systems now representing a new standard of care. These systems have profoundly reduced the burden of the disease and improved health outcomes, but they remain a management solution, not a cure.

Looking to the future, research efforts have shifted to a more fundamental objective: addressing the root cause of the disease. The development of immunotherapies like teplizumab, which can delay the onset of T1D, is a crucial first step toward halting the autoimmune attack. Simultaneously, groundbreaking work in stem cell-derived therapies is demonstrating the potential to replace the destroyed beta cells entirely. The ultimate success of these therapies will likely depend on their combined application. A functional cure will require not only the ability to replace insulin-producing cells but also the means to protect them from a misguided immune system. This synergy of research—in which new treatments are developed to both replace cells and reprogram the immune system—represents the most promising path toward a future where T1D is no longer a relentless, lifelong burden.

Works cited

1. Type 1 Diabetes Causes – Breakthrough T1D, accessed August 9, 2025, https://www.breakthrought1d.org/t1d-basics/causes/
2. www.mayoclinic.org, accessed August 9, 2025, https://www.mayoclinic.org/diseases-conditions/type-1-diabetes/symptoms-causes/syc-20353011#:~:text=The%20exact%20cause%20of%20type,Genetics
3. ​Risk of type 1 diabetes may depend on where childhood is spent, accessed August 9, 2025, https://timesofindia.indiatimes.com/life-style/health-fitness/health-news/risk-of-type-1-diabetes-may-depend-on-where-childhood-is-spent/photostory/123075027.cms
4. Genetics of the HLA Region in the Prediction of Type 1 Diabetes …, accessed August 9, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3233362/
5. Extreme genetic risk for type 1A diabetes – PNAS, accessed August 9, 2025, https://www.pnas.org/doi/10.1073/pnas.0606349103
6. Environmental Triggers of Type 1 Diabetes – PMC – PubMed Central, accessed August 9, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3385937/
7. Acute and Chronic Adverse Outcomes of Type 1 Diabetes – PubMed, accessed August 9, 2025, https://pubmed.ncbi.nlm.nih.gov/38272591/
8. Diabetic ketoacidosis – Symptoms & causes – Mayo Clinic, accessed August 9, 2025, https://www.mayoclinic.org/diseases-conditions/diabetic-ketoacidosis/symptoms-causes/syc-20371551
9. Diabetes-Related Ketoacidosis (DKA): Symptoms & Treatment, accessed August 9, 2025, https://my.clevelandclinic.org/health/diseases/21945-diabetic-ketoacidosis-dka
10. Complications of diabetes | Type 1 and Type 2 diabetes, accessed August 9, 2025, https://www.diabetes.org.uk/about-diabetes/looking-after-diabetes/complications
11. Diabetes, Eyes, Heart, Nerves, Feet and Kidneys, accessed August 9, 2025, https://www.kidney.org/sites/default/files/11-10-0216_ibe_diabetes-eyes-heart-nerves-feet-kidneys.pdf
12. Diabetes and Your Eyes, Heart, Nerves, Feet, and Kidneys …, accessed August 9, 2025, https://www.kidney.org/kidney-topics/diabetes-and-your-eyes-heart-nerves-feet-and-kidneys
13. 100 years of insulin – Penn Today – University of Pennsylvania, accessed August 9, 2025, https://penntoday.upenn.edu/news/100-years-insulin
14. The History of a Wonderful Thing We Call Insulin | American …, accessed August 9, 2025, https://diabetes.org/blog/history-wonderful-thing-we-call-insulin
15. Who discovered insulin? | Diabetes research, accessed August 9, 2025, https://www.diabetes.org.uk/our-research/about-our-research/our-impact/discovery-of-insulin
16. The Evolution of Insulin and How it Informs Therapy and Treatment Choices – PMC, accessed August 9, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC7366348/
17. History of diabetes: early science, early treatment, insulin, accessed August 9, 2025, https://www.medicalnewstoday.com/articles/317484
18. Insulin, Medicines, & Other Diabetes Treatments – NIDDK, accessed August 9, 2025, https://www.niddk.nih.gov/health-information/diabetes/overview/insulin-medicines-treatments
19. New immunotherapy drug could slow type 1 diabetes – UCLA Health, accessed August 9, 2025, https://www.uclahealth.org/news/article/new-immunotherapy-drug-could-slow-type-1-diabetes
20. Type 1 diabetes – Diagnosis and treatment – Mayo Clinic, accessed August 9, 2025, https://www.mayoclinic.org/diseases-conditions/type-1-diabetes/diagnosis-treatment/drc-20353017
21. Manage Blood Sugar | Diabetes – CDC, accessed August 9, 2025, https://www.cdc.gov/diabetes/treatment/index.html
22. Blood sugar testing: Why, when and how – Mayo Clinic, accessed August 9, 2025, https://www.mayoclinic.org/diseases-conditions/diabetes/in-depth/blood-sugar/art-20046628
23. Continuous Glucose Monitoring (CGM) – American Diabetes Association, accessed August 9, 2025, https://diabetes.org/advocacy/cgm-continuous-glucose-monitors
24. What are Automated Insulin Delivery Systems? | Medtronic, accessed August 9, 2025, https://www.medtronicdiabetes.com/treatments/automated-insulin-delivery
25. How to Count Carbs for Diabetes | Carb Calculator & Meal Planning, accessed August 9, 2025, https://diabetes.org/food-nutrition/understanding-carbs/carb-counting-and-diabetes
26. Key Points from the Updated Guidelines on Exercise and Diabetes – PMC, accessed August 9, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC5317029/
27. Exercising with Type 1 Diabetes: How to Work Out and Stay Safe – Healthline, accessed August 9, 2025, https://www.healthline.com/health/severe-hypoglycemia/working-out
28. Diabetes management: How lifestyle, daily routine affect blood sugar – Mayo Clinic, accessed August 9, 2025, https://www.mayoclinic.org/diseases-conditions/diabetes/in-depth/diabetes-management/art-20047963
29. Living with Diabetes – CDC, accessed August 9, 2025, https://www.cdc.gov/diabetes/living-with/index.html
30. Immunotherapy – Diabetes research, accessed August 9, 2025, https://www.diabetes.org.uk/our-research/immunotherapy
31. Cancer research discovery shows promising results in diabetes …, accessed August 9, 2025, https://timesofindia.indiatimes.com/life-style/health-fitness/health-news/cancer-research-discovery-shows-promising-results-in-diabetes-prevention-and-treatment/articleshow/123073886.cms
32. Islet Cell Replacement and Regeneration for Type 1 Diabetes: Current Developments and Future Prospects – PubMed Central, accessed August 9, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC11906537/
33. Islet Transplant for Type I Diabetes | Conditions & Treatments – UCSF Health, accessed August 9, 2025, https://www.ucsfhealth.org/treatments/islet-transplant-for-type-i-diabetes
34. A new therapy for treating Type 1 diabetes | Harvard Stem Cell …, accessed August 9, 2025, https://www.hsci.harvard.edu/news/new-therapy-treating-type-1-diabetes
35. Research hot topics – what are type 1 diabetes immunotherapies?, accessed August 9, 2025, https://www.diabetes.org.uk/our-research/about-our-research/hot-topics/immunotherapy/what-are-immunotherapies