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Type 1 Diabetes

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About the Disease

What is type 1 diabetes?slides Type 1 diabetes (T1D), also called autoimmune diabetes, results from mistaken recognition of islets of Langerhans, the only source of insulin in the body, as a foreign entity by the individual's own immune system. As a consequence, different cell types of the immune led by T cells work together to invade the pancreas and destroy pancreatic islets, leading eventually to their destruction and insulin deficiency. Before the discovery of insulin almost 100 years ago, T1D was invariably fatal due to hyperglycemia and ketosis. Insulin therapy has therefore been life saver for T1D patients. However, insulin replacement is not a cure and needs to be used on regular basis and on demand as advised by physicians. In addition, patients need to manage their blood sugar level 24/7, carefully watch their diets and follow certain regiments to avoid bouts of hypoglycemia and hyperglycemia and long term complications. Achieving this goal, however, is not easy, especially among young diabetic patients and kids. For these reasons, scientists around the globe, including our own group here at Hopkins, have been working around the clock to understand the disease pathogenesis and develop strategies to prevent or arrest the disease at onset.

Meet Our Research Team +

We are a team of lab scientists, biomedical researchers and patient care providers united in a desire to better understand diabetes processes.

Group Photo 2016

Biomedical investigators: Our team of basic scientists is led by Dr. Abdel Rahim Hamad and his talented postdoctoral fellows: Drs. Rizwan Ahmed, Anil Jaiswal, Mohanraj Sadasivam, and Yang Shen

Clinical investigators: Our team of clinical investigators is led by Dr. Thomas Donner, the director of the Diabetes Center at JHU and Ms. Sarah Lonegnecker, Research program coordinator.

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Learn about Our Research +

Our research team is working in harmony with other scientists and organizations to determine whether targeting a molecule called Fas ligand will interrupt disease progression and protect high risk individuals and may stop the disease at its track at on-set. This approach is based on solid data in mouse model of the disease. Now we are working diligently to determine how relevant the information we gathered in the mouse model is relevant to the human disease. We are using donated organs provided by the Network of Pancreatic organ donors with diabetes (nPOD), fresh blood samples from patients here at Hopkins and Samples provided by our collaborators at other institutes in US and Italy.

Dr. Rizwan Ahmed removing cell cultures from the CO2 chamber
Dr. Rizwan Ahmed removing cell cultures from the CO2 chamber

The data we are collecting from patients is encouraging and corroborates our hypothesis. Specifically, we see significant elevation of B lymphocytes expressing FasL among splenocytes of T1D subjects, but not healthy controls or at high-risk individual who have not yet developed over diabetes. Currently, we are working on characterization of these cells to understand more about their role in the disease process. If we find this also occurs in humans, it can provide a modulator whose blockade will not suppress the immune system and hence will be suitable for use in young individuals. For our published research, please visit our publications.

Dr. Rizwan Ahmed and his assistant Ben Cornwell transferring cells in the sterile hood.
Dr. Rizwan Ahmed and his assistant Ben Cornwell transferring cells in the sterile hood.

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Frequently Asked Questions +

What should you do if you are a parent of a child with T1D?
Because T1D leads to loss of insulin-producing beta cells in the pancreas, patients become dependent on receiving insulin injection on a daily basis to keep their glucose levels within a normal range. In addition, patients need to follow a proper eating regime. Failure to follow these procedures can lead to hypoglycemia which can lead in the short term to loss of concentration and delirium and in the long term to serious side effects, including renal failure and cardiac complications. Therefore, constant consultation with your child's physician is critical in guiding parents through these life changing events. For detailed response, please visit the JDRF website and those of your doctor's hospital.

How can you tell who is at risk of developing T1D?
As a result of the efforts led by the late George Eisenbarth, a simple blood screen test that detects autoantibodies against islet autoantigens is now routinely used to identify individuals who are at risk of developing T1D. This test is particularly useful for screening relatives of T1D patients and those carrying HLA susceptible genes. Doing this screening is useful for properly monitoring and for preparing at risk individuals for the possibility of contracting the disease. In addition, it may help them in following a healthy eating regimen to keep the disease at bay as long as possible. Once a patient knows that he/she is at risk of developing T1D, the individual may be eligible to sign up to participate in NIH clinical trials.

Is prevention of T1D possible?
We believe that any ailment can be cured or controlled, including T1D. Insulin is not a cure and there must be a better choice. Therefore, the current pressing question is how to protect at risk individuals. Scientists around the globe are working to develop modalities that can protect high-risk individuals from contracting the disease and to reverse it in newly diagnosed patients. Discovery of successful biological reagents that can be used to protect high risk individuals will significantly ease the pain of parents whose children are at risk and will eventually significantly lower the disease incidence. Such modalities should not impair patient's host defenses and need not be used periodically in new-onset patients.

Is prevention of T1D a realistic goal?
Yes. Significant advances have been made in understanding the disease process using mouse model. In addition, a large number of modalities can completely prevent the disease in mice and some even reverse the disease after its onset in the NOD mouse model. The challenge facing investigators is how to convert this wealth of knowledge into successful immunotherapies. This process has been underway for several years now. Although the results so far have been less than satisfactory, the efforts are continuing tirelessly at several fronts. These include: (1) Analysis of collected data to understand why the outcomes of recent trials were not more robust. (2) Efforts to identify new targets in mice and assessing their relevance to the human disease. (3) Analysis of the disease process directly in humans, which is critical to bridge the gaps in our understanding the disease process in mice.

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