The heterogeneous pathogenesis of autoimmune T1D is characterised by factors related to a person's genetics and their environment. Whilst key autoantigens have been identified, the initial triggers of the autoimmune T1D immune response remain uncertain.3

<h3>Autoimmunity and beta-cell destruction</h3>

The pathogenesis of autoimmune T1D begins when autoreactive T cells recognize and destroy pancreatic beta cells. This leads to a critical decline in insulin levels, which in turn causes ineffective control of blood glucose levels. Eventually, the remaining beta cells become insufficient to maintain normal blood glucose, reducing insulin secretion and leading to autoimmune T1D.4

<h3>Autoantigens and immune response</h3>

Autoimmune T1D patient´s immune system erroneously identifies specific beta cell components as autoantigens and attacks them.5 These T1D autoantigens can include6
<ul>
 <li>insulin B chain peptide (11-23)</li>
 <li>other beta-cell components such as GAD65, an enzyme associated with secretory vesicles</li>
 <li>protein phosphatase like IA-2</li>
</ul>
The presence of autoantibodies against these antigens serves as an important biomarker for disease progression, which is exponentially increased by any additional autoantibodies.6 Early detection of presymptomatic stages through screening for autoantibodies provides us with an opportunity to intervene, delay, and potentially prevent the symptomatic manifestation of autoimmune T1D.2

A potential mechanism for triggering autoimmune response4&nbsp;

When it comes to genetic factors, autoimmune T1D is strongly associated with specific HLA class II chain alleles which confer a higher risk for autoimmune T1D development.6
It is noteworthy that people living with other associated autoimmune diseases, such as celiac disease and autoimmune thyroid disease, are at an increased risk of developing autoimmune T1D than the general population.7
Does your patient have an existing autoimmune condition? Learn more about <a href="${link:{uuid:{bb90e1f3-ac46-45f4-8892-4883f3ac2ccc},repository:{articles},path:{/Global/indications/t1d/check-for-autoimmune-type-1-diabetes}}}">genetic risk factors linked to autoimmune T1D</a>.

<h3>Metabolic consequences of insulin deficiency</h3>

The destruction of pancreatic beta-cells due to autoimmune T1D results in insulin deficiency. Insulin deficiency, coupled with increased counterregulatory hormones, triggers the release of free fatty acids from adipose tissue. These fatty acids are then oxidized in the liver to form ketone bodies, leading to diabetic ketoacidosis (DKA), which ultimately causes worsening of hyperglycemia.8 DKA is a life-threatening condition often associated with high mortality, morbidity, and healthcare expenditure.9 <a href="${link:{uuid:{8ba6793a-69c0-4421-8153-21249585cfee},repository:{articles},path:{/Global/indications/t1d/early-detection-of-autoimmune-type-1-diabetes-could-reduce-the-risk-of-diabetic-ketoacidosis}}}">Early screening and detection of autoimmune T1D is therefore crucial for preventing DKA</a>.

<h2>Stages of autoimmune T1D progression</h2>

There is a trigger event that initiates the pathogenesis of autoimmune T1D before it progresses through four stages and eventually results in symptomatic autoimmune T1D. An initial immune response occurs during this trigger event with the development of a single autoantibody. As soon as additional autoantigens are detected, the number of beta cells is already shrinking. However, the pace at which autoimmune T1D progresses from the first autoimmune reaction to symptomatic disease varies from individual to individual and can take anywhere from a few months to decades.2,9

<h3>Stage 1. Early autoimmunity and beta-cell decline</h3>

The first stage of a beginning autoimmunity is characterized by the presence of two or more autoantibodies against the pancreatic islets in the peripheral circulation. In this stage the functional impairment and reduction of beta-cells is already in progress, but the number is still sufficient to maintain normoglycemia. That is why no symptoms are apparent yet.2

<h3>Stage 2. Progressive beta-cell dysfunction</h3>

In stage 2, the destruction of the beta-cells progressively increases, resulting in the decrease of insulin production. Glycaemic control can no longer be maintained, which eventually leads to dysglycemia. Although still pre-symptomatic, the autoantibodies remain detectable in the peripheral circulation at this stage as a biomarker for autoimmunity.2

<h3>Stage 3. Clinical symptoms and insulin dependence</h3>

At this stage, the destruction of the beta-cells has reached a degree at which insulin production is no longer sufficient to keep the blood sugar stable. Patients at this stage now show the typical clinical symptoms of autoimmune T1D, such as polyuria, polydipsia, weight loss, fatigue, and diabetic ketoacidosis (DKA). Hyperglycemia also occurs at this point, which makes an insulin medication unavoidable.2

<h3>Stage 4. Long-standing autoimmune T1D</h3>

At stage 4, patient has long-standing autoimmune T1D after living with the condition for several years and is insulin dependent.10-11 Long-term health complications are common, and two or more autoantibodies may or may not be detected in the blood at stage 4 autoimmune T1D.11

<h2>Early detection and progression of autoimmune T1D</h2>

Due to the latest research evidence on pathophysiological mechanisms in the development of autoimmune T1D, it is now possible to screen patients in the presymptomatic stages (1 and 2) for suspicious autoantibodies. This provides the opportunity to intervene, delay and ultimately prevent the natural progression of autoimmune T1D, preserving beta cell function.2,12

<h3>Early identification of autoimmune T1D</h3>

Currently, first- or second-degree relatives of individuals with autoimmune T1D or pediatric population are being screened for increased risk of developing autoimmune T1D in the research setting.2 The improved understanding of the development and progression of autoimmune T1D enables early detection, utilising autoantibody screenings as a primary tool. It opens a variety of possibilities for patients and their relatives as well as for HCPs in their care.13
<h2>Learn more about <a href="${link:{uuid:{efa3fba3-4d30-4f15-bc79-a5c9cac2ba1d},repository:{articles},path:{/Global/indications/t1d/test-for-autoantibodies}}}">how autoantibodies can be used to screen for T1D</a></h2>

Autoimmune type 1 diabetes (autoimmune T1D) is a progressive autoimmune disorder that causes the destruction of insulin-producing beta cells in the pancreas, leading to an inability to regulate blood glucose levels.1 Understanding the pathophysiology of autoimmune T1D can help identify potential at-risk patients and facilitate early intervention.2

The pathophysiology of autoimmune type 1 diabetes

TYPE-1-DIABETES

DIABETES

The incidence of autoimmune T1D is growing worldwide,1 making the disease an increasingly important topic for HCPs. Patients can develop comorbidities and severe complications, such as life-threatening diabetic ketoacidosis, which can significantly diminish their quality of life.1
Learn more about these impacts from <a href="${link:{uuid:{df323a59-7a2d-4bf2-ba62-4751c29e540b},repository:{articles},path:{/Global/indications/t1d/real-life-stories-from-people-living-with-autoimmune-t1d}}}">real-life stories of people living with autoimmune T1D</a>.
Autoimmune T1D manifests in children and adolescents.1,4 However, an estimated 50% of new cases emerge in adults.5 Autoimmune T1D is often misdiagnosed as type 2 diabetes, complicating estimations of incidence rates.4,5

It is a progressive autoimmune disease characterized by the destruction of insulin-producing pancreatic beta cells. Early identification can help monitor disease progression and implement preventive measures before <a href="${link:{uuid:{efa3fba3-4d30-4f15-bc79-a5c9cac2ba1d},repository:{articles},path:{/Global/indications/t1d/test-for-autoantibodies}}}" target="_self">autoimmune</a> T1D onset.1,4,11 B cells produce autoantibodies against islet cells and activate T cells that target pancreatic cells.1,4 However, the exact causes of autoimmune T1D are not yet clearly identified.12
Learn more about the complex pathogenesis and pathophysiology of autoimmune T1D.

A mix of genetic and environmental risk factors likely trigger islet autoimmunity and development of autoimmune T1D and may also vary with age of disease onset. For example, increased inflammation detected in those who develop autoimmune T1D at a younger age might be one factor contributing to the heterogeneity of the disease.13

<h3>Genetic risk factors for autoimmune type 1 diabetes</h3>

Having a relative with autoimmune T1D is a risk factor. The risk of developing autoimmune T1D is between 1 in 300 to 1 in 250.* This risk increases to 1 in 40 to 1 in 35 for those with parents who have the disease. However, the majority of patients do not have a family history of the disease.14
Shared genetic risk factors are potentially implicated both in polyautoimmunity (occurrence of ≥2 autoimmune diseases in a single patient) and family autoimmunity (presence of ≥2 autoimmune diseases in members of a nuclear family) among individuals with autoimmune T1D.15
Human leukocyte antigen (HLA) plays a role in fighting pathogens. HLA genes encoding DR and DQ are also associated with a high risk of autoimmune T1D and therefore considered genetic risk factors for autoimmune T1D.16 The genotypes are detected in 90% of pediatric autoimmune T1D patients.17 Dysregulation of other genes such as cytotoxic T cell-associated protein 4 (CTLA-4) and protein tyrosine phosphatase, nonreceptor type 22 (PTPN22) might also contribute to the onset of autoimmune T1D.18
*based on a US population

<h3>Environmental risk factors for autoimmune T1D</h3>

Some studies suggest a link between infections and autoimmune T1D.1,14 For example, recent research suggests that SARS-CoV-2 increases the risk of autoimmune T1D and accelerates the progression of the disease.12 Enteroviruses and bacterial infections have also been implicated in other studies. However, further validation is required to confirm a causal relationship.12
Other risk factors for autoimmune T1D have been proposed, including exposure to toxins and maternal diet.19,20 However, the evidence presented in these studies is often weak and/or inconclusive. 19,20

<h3>Autoimmune conditions as risk factors for autoimmune T1D</h3>

Autoimmune T1D shows a genetic overlap with several autoimmune conditions. For instance, Addison's disease is associated with a higher risk of autoimmune T1D.21 Furthermore, patients with celiac and autoimmune thyroid disease have an estimated 4-9% and 15–30% increased risk, respectively, of developing autoimmune T1D.22
There is also a familial link between autoimmune T1D and autoimmune disease.2 &nbsp;First-degree relatives of individuals with other autoimmune diseases including celiac and thyroid diseases may also be more likely to develop &nbsp;autoimmune T1D.2
Learn more about the link between <a href="${link:{uuid:{bb90e1f3-ac46-45f4-8892-4883f3ac2ccc},repository:{articles},path:{/Global/indications/t1d/check-for-autoimmune-type-1-diabetes}}}" target="_self">autoimmune T1D and autoimmune disease</a>.

<h3>Obesity and diet as risk factors for autoimmune T1D</h3>

Obesity and autoimmune T1D are correlated. Obesity possibly contributes to the disease by increasing insulin resistance and causing systemic inflammation.23
The intake of certain nutrients has also been associated with a higher risk for the development of autoimmune T1D. For instance, research suggests that high sugar consumption can promote the progression of autoimmune T1D.24
Other potential nutritional risk factors for autoimmune T1D, such as gluten, have also been investigated. However, the studies are inconsistent with contradictory results.14

<h3>Psychological stress as a risk factor for autoimmune T1D</h3>

There may be a link between stress and the risk of autoimmune T1D.
For instance, mothers encountering a significant life event during pregnancy may increase the risk of their child developing autoimmune T1D.25,26
Additionally, some studies suggest that children who are exposed to excessive psychological stress, such as the divorce of their parents or experience of violence, have an increased risk of autoimmune T1D.14
Modifiable factors like nutritional intake and stress may contribute to the development of autoimmune T1D, potentially providing strategies to delay or prevent onset of the disease. However, in many cases, additional robust evidence is required before evidence-based recommendations can be made.14,24
In conclusion, early identification of individuals with islet autoantibodies before the clinical onset of T1D allows for the timely implementation of preventive measures and treatments that could prevent the natural progression of autoimmune T1D and preserve beta cell function.11

<h2>Learn more about how autoimmune type 1 diabetes can be detected years before symptom onset</h2>

The causes and risk factors of autoimmune type 1 diabetes (autoimmune T1D) are multifactorial. A combination of genetic susceptibility and other risk factors, like a family history of autoimmune disease, increase the risk of developing the pathology.1,2 Identifying these risk factors can help HCPs proactively screen high-risk patients and help avoid serious complications through targeted interventions.3

Etiology and risk factors for autoimmune type 1 diabetes

<h2>Why are autoantibodies important in autoimmune T1D screening?</h2>

Autoantibodies are measurable biomarkers that appear months or even years before symptoms of autoimmune T1D develop and serve as key indicators of early beta-cell destruction.4 Screening for these biomarkers allows for the early identification of individuals at risk of developing autoimmune T1D, enabling caregivers to prepare for timely intervention and potentially preventing or delaying the onset of the disease.1,5
Blood tests like the diabetes mellitus autoantibody panel (also called the islet autoantibody test) can detect autoantibodies targeting insulin-producing cells, helping to differentiate autoimmune T1D from other forms.6 This early detection is particularly critical because autoimmune T1D progresses in distinct stages, often leading to significant beta-cell loss by the time symptoms appear.1
Many individuals with a single autoantibody do not progress to autoimmune T1D. However, the presence of two or more autoantibodies increases the risk of progression to clinical autoimmune T1D to 70% over 10 years and 100% over a lifetime.2,7
The autoantibodies detected in autoimmune T1D include:
<ul>
 <li>Glutamic Acid Decarboxylase Antibodies (GADA)8</li>
 <li>Insulinoma-associated-2 Autoantibodies (IA-2A)8</li>
 <li>Insulin Autoantibodies (IAA)8</li>
 <li>Zinc Transporter 8 Autoantibodies (ZnT8A)8</li>
</ul>
Screening for these offers significant insight into the pathogenesis of immune-mediated diabetes. Learn more about the clinical significance of these <a href="${link:{uuid:{efa3fba3-4d30-4f15-bc79-a5c9cac2ba1d},repository:{articles},path:{/Global/indications/t1d/test-for-autoantibodies}}}">autoantibodies in autoimmune T1D</a>.
The presence of multiple autoantibodies not only confirms the likelihood of beta-cell destruction but also significantly enhances the ability to predict autoimmune T1D progression. Screening panels that identify two or more autoantibodies offer an accurate assessment of risk, helping to identify individuals who may benefit from closer monitoring and potential intervention.2
<h3>Risk of progression to autoimmune T1D after seroconversion to islet autoantibody positivity7</h3>

Early screening for type 1 diabetes autoantibodies enables the identification of individuals at risk before symptoms appear, allowing for timely intervention and disease management.1 Anti-islet autoantibodies that target proteins associated with beta-cells serve as biomarkers of autoimmune type 1 diabetes (autoimmune T1D) development.2 The number of detectable autoantibodies through screening correlates with the risk of developing autoimmune T1D.2 Assays for detecting autoimmune T1D have shown high sensitivity and specificity.3

Screening for autoimmune type 1 diabetes using autoantibodies

<h2>What is the difference between autoimmune type 1 vs type 2 diabetes screening?</h2>

Type 1 diabetes is an autoimmune disease-causing islet cell destruction, while type 2 diabetes results from insulin resistance. Due to these differences, screening for aT1D and type 2 diabetes varies in target populations, tests, frequency, and goals.9
<table border="1" cellpadding="10" cellspacing="1" style="height:100%;width:100%;">
 <tbody>
 <tr>
 <td style="width: 20%; text-align: center;">Parameters</td>
 <td style="width: 50%;">
 Autoimmune T1D</td>
 <td style="width: 30%; text-align: center;">T2D</td>
 </tr>
 <tr>
 <td style="width: 20%;">Target populations&nbsp;</td>
 <td style="width: 50%;">Children and adolescents, especially those with a family history of autoimmune T1D or other autoimmune conditions. Rising incidence in children under five. Adults over 18 can also develop autoimmune T1D at equal rates.1</td>
 <td style="width: 30%;">Adults, particularly those with risk factors such as obesity, hypertension, physical inactivity, or a family history of T2D.9</td>
 </tr>
 <tr>
 <td style="width: 20%;">Screening tests and biomarkers</td>
 <td style="width: 50%;">Autoantibody tests, such as the diabetes mellitus autoantibody panel, to detect markers of autoimmune beta-cell destruction.8</td>
 <td style="width: 30%;">Fasting plasma glucose, A1C, HbA1c, and oral glucose tolerance tests to assess insulin resistance and glucose metabolism.9</td>
 </tr>
 <tr>
 <td style="width: 20%;">Frequency of screening</td>
 <td style="width: 50%;">Children with a family history of autoimmune disease should be screened every 3 years to annually until age 18. Adults generally require no additional screening unless symptomatic. Positive results require follow-up with a diabetes expert, with children monitored at intervals and adults screened every 3-5 years only if there’s a family history of autoimmune disease.11</td>
 <td style="width: 30%;">Screening is recommended every 3 years if normal results are found, especially for those aged 40-70 who are overweight or obese. Those with multiple risk factors may need annual or more frequent tests.9</td>
 </tr>
 <tr>
 <td style="width: 20%;">Screening goals</td>
 <td style="width: 50%;">Identify high-risk individuals through diabetes-related autoantibody testing to enable early interventions or clinical trial opportunities to preserve beta-cell function and delay disease onset.11</td>
 <td style="width: 30%;">Identify asymptomatic individuals at risk to enable early interventions (lifestyle changes, medications) that can delay disease progression and reduce adverse outcomes like cardiovascular disease.9</td>
 </tr>
 </tbody>
</table>

<h2>What is the right age for autoimmune screening?</h2>

Although autoimmune T1D can manifest at any age, it most commonly occurs in children, teenagers, or young adults.1 Autoantibodies often emerge before the age of 6, even in cases where autoimmune T1D is diagnosed much later in childhood. Screening for islet autoantibodies at ages of 2 and 6 has proven to be sensitive and efficient in predicting autoimmune T1D.12
Current <a href="https://diabetesjournals.org/care/article/47/Supplement_1/S52/153956/4-Comprehensive-Medical-Evaluation-and-Assessment" target="_blank">type 1 diabetes guidelines</a> provide specific recommendations on the age ranges and risk factors for autoimmune T1D screening.

<h2>What are the benefits of early screening for autoimmune T1D?</h2>

Early screening for autoimmune T1D autoantibodies in individuals at risk, such as those with a family history of autoimmune T1D or related autoimmune conditions like celiac disease offers critical advantages.11 Learn more about etiology and risk factors for autoimmune T1D.
Early detection presents a significant opportunity to prevent the natural progression of autoimmune T1D and preserve beta cell function.5
Screening shows that approximately 95% of relatives of individuals with autoimmune T1D test negative for autoantibodies, which can provide reassurance, especially to families with an affected member.13
In individuals who test positive for autoantibodies, screening leads to early detection of autoimmune T1D7, which in turn provides critical advantages, such as:

<h3>Prevention of misdiagnosis and delayed treatment</h3>

Autoimmune T1D screening helps prevent misdiagnosis and delayed treatment by identifying the disease in adults, where it is often misdiagnosed, especially in those not requiring insulin at diagnosis. Early detection allows for proper staging, preserving endogenous insulin production, and enabling timely access to therapies like immunotherapy, especially in individuals with a family or personal history of autoimmune conditions.11

<h3>Early treatment and glycemic control</h3>

Autoimmune T1D screening contributes to glycemic control by allowing early interventions that address challenges such as the loss of counterregulatory mechanisms and hypoglycemia unawareness. Early diagnosis helps manage these risks more effectively and supports treatments that maintain target blood sugar levels while minimising the risk of hypoglycemia and associated barriers.1

<h3>Reduced risk of diabetic ketoacidosis (DKA) at diagnosis</h3>

<a href="${link:{uuid:{8ba6793a-69c0-4421-8153-21249585cfee},repository:{articles},path:{/Global/indications/t1d/early-detection-of-autoimmune-type-1-diabetes-could-reduce-the-risk-of-diabetic-ketoacidosis}}}">Detecting multiple T1D autoantibodies early reduces the risk of life-threatening complications like diabetic ketoacidosis (DKA)</a> at symptom onset.7

<h3>Preparing patients and families for autoimmune T1D management</h3>

Early screening provides patients and their families with valuable time to prepare for autoimmune T1D, enabling a smoother transition if symptoms develop.7 Uncover the <a href="${link:{uuid:{df323a59-7a2d-4bf2-ba62-4751c29e540b},repository:{articles},path:{/Global/indications/t1d/real-life-stories-from-people-living-with-autoimmune-t1d}}}">real-life stories of patients living with autoimmune T1D</a>.

<h2>How should individuals with positive autoimmune T1D autoantibodies be monitored over time?</h2>

Learn more about <a href="${link:{uuid:{19a27d0f-8329-4fe1-aaff-df0b85ef49ac},repository:{articles},path:{/Global/indications/t1d/how-should-individuals-with-positive-autoimmune-t1d-autoantibodies-be-monitored-over-time}}}">how to monitor individuals with positive autoantibodies over time</a> and download our <a href="${link:{uuid:{4a539dff-fd95-405c-ac7b-a9bf8f0beb0e},repository:{dam},path:{/Portal/Global/t1d/resources/MAT-GLB-2405090_Sanofi_Tzield_Infographic_3_Who-to-Screen_Digital.pdf}}}">resource on who to screen</a> for further guidance.

Early screening for type 1 diabetes autoantibodies enables the identification of individuals at risk before symptoms appear, allowing for timely intervention and disease management.1 Anti-islet autoantibodies that target proteins associated with beta-cells serve as biomarkers of autoimmune type 1 diabetes (autoimmune T1D) development.2 The number of detectable autoantibodies through screening correlates with the risk of developing autoimmune T1D.2 Assays for detecting autoimmune T1D have shown high sensitivity and specificity.3

The progression of autoimmune type 1 diabetes (T1D) is gradual, often detectable months or even years before symptoms arise.1–3 Through proactive screening, we can identify the condition well in advance.3 Meet our ambassadors living with autoimmune T1D and discover the risk factors to look out for when considering who to screen.

Real-life stories from people living with autoimmune T1D 

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Real-life stories from people living with autoimmune T1D

The latest articles

The pathophysiology of autoimmune type 1 diabetes

Etiology and risk factors for autoimmune type 1 diabetes

Screening for autoimmune type 1 diabetes using autoantibodies

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What is autoimmune T1D?

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