How Does Diabetes Suppress The Immune System?

How Does Diabetes Suppress The Immune System
4. Diabetes Leads to Decreased Complement Response – The complement system is an integral part of our immune system. It enhances the ability of antibodies and phagocytic cells to fight disease causing germs and eliminate them from our body. However, hyperglycemia or high blood sugar causes defects in complement receptors and impairs their ability to cause phagocytosis.

Why does diabetes cause immunosuppression?

This low and chronic inflammation damages the pancreatic beta cells and leads to insufficient insulin production, which results in hyperglycemia. Hyperglycemia in diabetes is thought to cause dysfunction of the immune response, which fails to control the spread of invading pathogens in diabetic subjects.

Does diabetes mean you have a weak immune system?

Having diabetes isn’t what makes someone’s immune system weaker, but chronic high blood sugars and out-of-range numbers can weaken the immune system, leaving people more susceptible to illness and complications from illnesses.

Why does diabetes make you more susceptible to infection?

Why are people with diabetes more prone to infections? – High blood sugar levels can weaken a person’s immune system defenses. People who have had diabetes for a long time may have peripheral nerve damage and reduced blood flow to their extremities, which increases the chance for infection.

Does insulin suppress the immune system?

– Dr. Tsai and team were able to pinpoint an insulin signaling pathway that boosts the activity of T cells, allowing them to quickly multiply and send out further signals, activating the rest of the immune system as necessary. ” We have identified one of metabolism’s most popular hormones, specifically the insulin signaling pathway, as a novel ‘co-stimulatory’ driver of immune system function.” Study co-author Dr.

  1. Daniel Winer “Our work characterizes the role of this signaling pathway in immune cells, mainly T cells, opening up avenues in the future to better regulate the immune system,” he explains.
  2. The researchers worked with mice that they genetically engineered to express T cells that did not have insulin receptors, so as to simulate insulin resistance.

To see how effective the T cells were, the scientists exposed them to different types of pathogens, including the H1N1 strand of flu, The research team found that the T cells without insulin receptors had weaker responses and needed more “danger” signals than usual in order to react to the threat.

This, explains Dr. Winer, is because “the insulin receptor or signaling molecule is like a second push to the immune system to ensure that it can fight off the infection with the best possible weapons it has.” When the immune cells were unable to “sense” insulin and respond to it, they were inefficient in fighting pathogens.

“T cells are at the heart of so many diseases,” notes Dr. Tsai. “If we can understand them at the cellular level, this will give us the best opportunity to find new pathways to target for new therapies.” The researchers believe that, in learning more about insulin’s immunity-boosting properties, we may, in the future, be able to use this knowledge to develop more effective treatments for inflammatory diseases, such as arthritis and Crohn’s disease,

Does metformin weaken immune system?

Abstract – Background: Metformin, a widely prescribed blood glucose normalizing antidiabetic drug, is now beginning to receive increasing attention due to its anti-inflammatory properties. Objective: To provide a critical and comprehensive review of the available literature describing the effects of metformin on the immune system and on auto-inflammatory diseases.

  1. Results: Based on the available scientific literature, metformin suppresses immune responses mainly through its direct effect on the cellular functions of various immune cell types by induction of AMPK and subsequent inhibition of mTORC1, and by inhibition of mitochondrial ROS production.
  2. Among key immune events, this results in inhibited monocyte to macrophage differentiation and restrained inflammatory capacity of activated macrophages.

In addition, metformin treatment increases differentiation of T cells into both regulatory and memory T cells, as well as decreasing the capacity of neutrophils to commence in NETosis. Due to its inhibitory effect on the proinflammatory phenotype of immune cells, metformin seems to reduce auto-immune disease burden not only in several animal models, but has also shown beneficial results in some human trials.

  1. Conclusions: Based on its immunomodulatory properties and high tolerability as a drug, metformin is an interesting add-on drug for future trials in treatment of immune mediated inflammatory diseases.
  2. Eywords: Metformin; RA; SLE; T lymphocytes; auto-immune disease; inflammation; macrophages; neutrophils.

Copyright© Bentham Science Publishers; For any queries, please email at [email protected]

Are diabetics more prone to colds?

Diabetes raises your risk of catching a cold or the flu because it weakens your immune system, And when you’re sick, it’s harder to keep blood sugars under control, While your body fights the illness, it releases hormones that increase blood sugars and interfere with insulin ‘s blood-glucose-lowering effects.

Is diabetes a side effect of immunosuppression?

Martha Walker, DPT, CSCS Chris L. Wells, PhD, PT, CCS, ATC At the time of your organ transplant, you were placed on a regimen of immunosuppressant medications to prevent your immune system from rejecting the donor organ. There are many different immunosuppressant medications you may have been prescribed, including corticosteroids, tacrolimus, cyclosporine, mycophenolate, azathioprine, and sirolimus.

These medications are vital for your new organ’s survival; however, many of them come with mild to severe unwanted side effects. But there are steps you can take to lessen their impact. One of the major side effects of corticosteroids is osteoporosis. Osteoporosis is when the density of your bones is decreased, increasing the risk for fractures.

Any bone in your body can be affected; however, fractures are most commonly seen at the hip, spine, or wrist. To learn more about osteoporosis, please go www.apta.org and search under osteoporosis (select the first option followed by selecting “body” which will bring you to a pamphlet on osteoporosis).

  • The effects of osteoporosis can be lessened through exercise, supplemental Vitamin D and calcium, and medications such as Fosomax and Boneva, which you can ask your doctor about.
  • It is important to engage in an exercise program that includes weight bearing activities and resistance training to maintain your bone density, and hopefully make your bones stronger and lessen the risk for fractures.

Weight bearing activities require your bones and muscles to work against gravity and absorb forces from the ground. This can be walking, jogging, stair climbing or dancing. Resistive training, which can include weight training with free weights, machines, or resistive bands, can also improve your muscle strength and therefore bone health particularly for the long thigh bone, femur.

  • The benefits of resistance training do not end at osteoporosis.
  • It can also improve your overall strength, balance and reaction time, putting you less at risk for falls.
  • Several immunosuppressant medications have been linked to a decrease in muscle function.
  • Tacrolimus and cyclosporine derived medications have been linked to a delay in muscle contraction, decrease in coordination between the different types of muscle fibers to efficiently contract and relax, and a decrease in the adaptability of muscle fibers to change to meet the demands we place upon our muscles.
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Corticosteroids also adversely affect muscle fibers, particularly the type two muscle fibers that contract rapidly to produce immediate force or power so we can respond quickly. Corticosteroids decrease muscle protein production and decrease the ability of the muscle to produce muscle energy in an effective manner.

  • Participating in a general exercise program that includes aerobic and resistive training appears to improve muscle function and decreases the adverse effects on the muscles.
  • Another side effect of immunosuppressant medications is hyperglycemia (high blood sugar) and secondary diabetes because they may alter the way your body manages glucose (sugar).

It is important to routinely check your blood sugar and work closely with an endocrinologist to establish an effective medication regimen to maintain stable blood sugar level that is close to normal, 80 to 120. Exercise can help lower your blood sugar and possibly decrease medications requirements.

Aerobic exercise such as walking, biking and swimming for 30 minutes four-five days a week is very helpful and can lead to an improvement in your health, along with resistive training to increase your muscle mass, which will improve your body’s ability to utilize glucose. Another way to decrease the adverse effects of hyperglycemia or diabetes is to improve your diet.

Most of us need to increase the amount of lean protein (chicken, fish and lean beef), vegetables, and whole grains that we eat. It is also important to limit your consumption of sweets. As with starting any diet and exercise program, it is important to check first with your physician and health care providers to obtain their input and advice.

Types : walking, jogging, biking, swimming, dancing
Duration : 30 minutes
Intensity : moderate level (experiencing shortness of breath but can still talk)
Frequency : 4-5 days a week

Table 2: Resistive Training

Upper Body Lower body
Military Presses: Sitting with good posture, raise your arms over head. Step Ups : Place one foot on a step, press up to transfer your weight onto the step, and then lower down slowly. Avoid using the other leg to push yourself up onto the step.
Shoulder Abduction: Sitting with good posture, raise your arms out to the side until shoulder height. Hip Abduction : Standing with good posture, lift your leg out to the side while keeping your hip and knee straight and your foot pointing straight ahead.
Push Ups: either from the floor or against the wall, lower your straight body to the floor or wall, then press up to straighten your arms. Hip Extension: Standing with good posture, lift your leg backwards while keeping your hip and knee straight, and your upper body still.
Heel Walking : while standing next to your kitchen counter for balance, lift your toes and front of foot off floor. Then walk the length of the counter on your heels.

Last Reviewed: 12/21/2021

What happens to the immune system in type 1 diabetes?

Cause – Glucose is a type of sugar that is absorbed into your bloodstream when you digest food. As the amount of glucose, or sugar in your blood goes up, clusters of special cells in your pancreas called beta-cells make insulin. Insulin is a hormone that works like a gatekeeper.

It allows glucose to move into the cells and tissues in your body, where it is used for energy and to help your organs function normally. With type 1 diabetes, your immune system attacks your insulin-producing beta-cells. Without these beta-cells, your body doesn’t have enough insulin. Without insulin, glucose can’t enter your cells and builds up in your blood, starving your cells.

Scientists don’t know what exactly causes the immune system to attack beta-cells. But genes seem to play a role, and other factors may act as a trigger.

How is diabetes related to autoimmune?

Abstract. – Type 1 diabetes (T1D) is an organ-specific autoimmune disease caused by the autoimmune response against pancreatic β cells. T1D is often complicated with other autoimmune diseases, and anti-islet autoantibodies precede the clinical onset of disease. The most common coexisting organ-specific autoimmune disease in patients with T1D is autoimmune thyroid disease, and its frequency is estimated at > 90% among patients with T1D and autoimmune diseases. The prevalence of anti-thyroid antibodies in children with T1D at disease onset is about 20% and is particularly common in girls. Furthermore, patients with anti-thyroid antibodies are 18 times more likely to develop thyroid disease than patients without anti-thyroid antibodies. Therefore, for early detection of autoimmune thyroid disease in children with T1D, measurement of anti-thyroid antibodies and TSH at T1D onset and in yearly intervals after the age of 12 yr is recommended. Anti-islet autoantibodies are predictive and diagnostic markers for T1D. The most frequently detected autoantibodies in Japanese patients are GAD autoantibodies (~80%) followed by IA-2 autoantibodies (~60%), insulin autoantibodies (~55%) and ZnT8 autoantibodies (~50%). In a combined analysis, 94% of Japanese patients with T1D can be defined as having type 1A diabetes. Furthermore, autoantibodies to ZnT8 and IA-2 are associated with childhood-onset and acute-onset patients. Thus, it is important to develop a diagnostic strategy for patients with type 1A diabetes in consideration of the age or mode of disease onset. Keywords: anti-islet autoantibodies, autoimmune thyroid disease, prediction, type 1 diabetes, Zinc transporter 8

Why does diabetes increase inflammation?

How Chronic Inflammation Impacts Your Blood Sugar – So what’s the connection between chronic inflammation and diabetes? It’s a bit complicated. Chronic inflammation is a risk factor for both type 1 and type 2 diabetes, but it can also be a complication of diabetes.

  1. In the case of type 1 diabetes, inflammation is part of the autoimmune response that causes the disease.
  2. Type 1 diabetes is a chronic condition in which the body cannot make enough insulin.
  3. Chronic inflammation from the body’s autoimmune response causes damage to the insulin producing cells in the pancreas, which leads to even more inflammation.

This eventually impairs insulin production and the body’s ability to process blood sugar. Although more research needs to be done, studies have found that inflammation in response to environmental factors, including inflammation from exposure to infections, may influence the development of type 1 diabetes.

Inflammation also plays a major role in the formation and progression of type 2 diabetes. Type 2 diabetes is chronic condition in which the body has difficulty processing glucose (aka blood sugar) from carbohydrates in food. This causes chronically high levels of blood sugar, which eventually triggers the body’s inflammatory response.

Over time, type 2 diabetes causes ongoing inflammation in the body. Inflammation is also a factor in developing type 2 diabetes. Studies have found that pro-inflammatory compounds can disrupt the insulin-signaling pathways involved in metabolizing glucose, thus contributing to type 2 diabetes.

What kind of infections do diabetics get?

Asymptomatic Bacteriuria – Asymptomatic bacteriuria is the presence of a pathogen in the urine of an asymptomatic patient. In 2005, the Infectious Diseases Society of America published guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults ( 27 ).

For asymptomatic women, bacteriuria is defined as two consecutive clean catch voided urine samples with the same bacterial strain in counts ≥10 5 cfu/mL ( 26 ) or a single catheterized urine specimen with one bacterial species isolated in counts ≥10 5 cfu/mL; the latter also defines bacteriuria in asymptomatic men ( 27, 28 ).

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The true incidence and prevalence of asymptomatic bacteriuria is unknown (especially in men) ( 27 ). Multiple studies show that asymptomatic bacteriuria is more common in women with diabetes ( 2, 5, 29 ). In one study, the prevalence of asymptomatic bacteriuria was 26% in women with diabetes compared with 6% in those without diabetes ( 23 ).

In another, the prevalence was 29% in women with diabetes, which was about three times greater than that in women without diabetes ( 30 ). Hypothesized reasons for this greater prevalence include urethral reflex and residual volume due to morphologic and functional changes in the bladder that results from diabetes ( 31 ).

In men with diabetes, the overall prevalence of asymptomatic bacteriuria is 1%–11% and is similar to that in men without diabetes ( 2 ). As mentioned, female sex is an independent risk factor for developing asymptomatic bacteriuria ( 32 ). In women with diabetes, diabetes duration of ≥10 years (relative risk 2.6, 95% CI 1.3–5.1) and use of insulin (RR 3.7, 95% CI 1.8–7.3), but not the level of glycemic control, increase the risk for developing the condition compared with age-matched women without diabetes ( 20 ).

  1. Diabetic neuropathy and nephropathy have been associated with asymptomatic bacteriuria in women with type 1 diabetes, but not type 2 diabetes ( 2 ).
  2. Escherichia coli remains the organism most commonly isolated in urine specimens, but other gram-negative organisms, such as Staphylococcus saprophyticus and enterococci, are also common.

Individuals with diabetes have an increased risk of developing symptomatic cystitis, pyelonephritis, and perinephric abscess (see the sections Cystitis and Pyelonephritis, Emphysematous Pyelonephritis, and Renal and Perinephric Abscess ). Though a few small studies suggest that asymptomatic bacteriuria can increase the risk for developing symptomatic UTI in women with diabetes, large-scale studies are needed to support this link ( 33, 34 ).

  1. Furthermore, studies evaluating the effect of antibiotic therapy on asymptomatic bacteriuria failed to show a change in long-term outcomes.
  2. In one study evaluating the effect of antibiotic therapy in adult women with diabetes and asymptomatic bacteriuria, during a mean follow-up of 27 months, 40% of women in the placebo group and 42% of women in the antimicrobial therapy group had at least one episode of symptomatic UTI ( 35 ).

The time to a first symptomatic episode was similar in the placebo group and the antimicrobial therapy group (p=0.67 by the log-rank test), as were the incidence rates (±standard deviation) per 1,000 days of follow-up of any symptomatic UTI (i.e., bacteriuria) (1.10±0.17 and 0.93±0.14, respectively; RR 1.19, 95% CI 0.28–1.81), pyelonephritis (0.28±0.08 and 0.13±0.05, respectively; RR 2.13, 95% CI 0.81–5.62), and hospitalization for UTI (0.10±0.36 and 0.06±0.22, respectively; RR 1.93, 95% CI 0.47–7.89) ( 33 ).

What happens when a diabetic gets an infection?

Because of the buildup of plaque in blood vessels associated with diabetes, areas of infection may receive a poor blood supply, further lowering the body’s ability to fight infections and heal wounds.

Does insulin suppress inflammation?

INSULIN MODULATES INFLAMMATORY MEDIATORS – The discovery of the anti-inflammatory effect of insulin can be traced back to the observation that insulin exerts a vasodilatory effect through endothelial NO release in arteries, veins and capillaries. By inducing vasodilatation, it reduces leukocyte adhesion to the endothelium and subsequent infiltration.

  1. Furthermore, it has inhibitory effects on platelet adhesion and aggregation.
  2. Studies have further confirmed that insulin suppressed three important inflammatory mediators: intercellular cell adhesion molecular-1 (ICAM-1), MCP-1 expression and NFκB binding in human aortic endothelial cells in vitro,
  3. These suppressive effects can be blocked by the NOS inhibitor N(G)-nitro-L-arginine, indicating the effects are mediated by NO release.

Among all the pro-inflammatory cytokines, TNF-α is the most active one in triggering the production of other cytokines such as IL-6 and other expression molecules. We provided direct evidence in myocardial ischemia/reperfusion (I/R) rats that insulin inhibits TNF-α induction locally and systemically, and demonstrated for the first time that in vitro treatment with insulin attenuated I/R-induced TNF-α production in cardiomyocytes via the Akt-eNOS-NO signaling pathway.

  • Polymorphonuclear neutrophils (PMN) are the first defense line against infection and invasive microorganisms.
  • Adherence of PMN to endothelial cells is an early requisite event in I/R-induced inflammatory injury.
  • Thus we performed in vivo and in vitro experiments in a rabbit model to investigate whether insulin inhibits PMN-mediated adherence.

It was found that insulin reduced P-selectin and ICAM-1 expression in endothelium which mediates the initial interaction between PMNs and the endothelial cell surface, thus insulin attenuated PMN adherence and I/R-induced inflammatory injury. The Akt-eNOS-NO signaling pathway was involved in these effects.

What happens when you suppress your immune system?

A suppressed immune system is weakened to the point that it cannot mount a proper immune response to protect the body from pathogens, such as bacteria, viruses, and other infectious microorganisms. Therefore, people with a suppressed immune system become vulnerable to various infectious diseases.

Why do diabetics not heal well?

High blood glucose levels – If you have diabetes, your body doesn’t know how to effectively control your blood glucose, or blood sugar, on its own. If your blood sugar levels are consistently high, it can lead to problems with circulation, nerves and immune system – all of which can get in the way of good wound healing.

What is the life expectancy after diabetes?

Life expectancy can be increased by 3 years or in some cases as much as 10 years. At age 50, life expectancy- the number of years a person is expected to live- is 6 years shorter for people with type 2 diabetes than for people without it. People with type 2 diabetes can reduce their risk of complications and live longer by achieving their treatment goals.

What is diabetes last stage?

– While “end-stage diabetes” isn’t a commonly used term, diabetes can lead to what’s known as end-stage diabetic complications, or advanced complications. In people with diabetes, advanced complications, like end-stage renal disease, occur after many years of living with diabetes.

How is diabetes related to autoimmune?

Abstract. – Type 1 diabetes (T1D) is an organ-specific autoimmune disease caused by the autoimmune response against pancreatic β cells. T1D is often complicated with other autoimmune diseases, and anti-islet autoantibodies precede the clinical onset of disease. The most common coexisting organ-specific autoimmune disease in patients with T1D is autoimmune thyroid disease, and its frequency is estimated at > 90% among patients with T1D and autoimmune diseases. The prevalence of anti-thyroid antibodies in children with T1D at disease onset is about 20% and is particularly common in girls. Furthermore, patients with anti-thyroid antibodies are 18 times more likely to develop thyroid disease than patients without anti-thyroid antibodies. Therefore, for early detection of autoimmune thyroid disease in children with T1D, measurement of anti-thyroid antibodies and TSH at T1D onset and in yearly intervals after the age of 12 yr is recommended. Anti-islet autoantibodies are predictive and diagnostic markers for T1D. The most frequently detected autoantibodies in Japanese patients are GAD autoantibodies (~80%) followed by IA-2 autoantibodies (~60%), insulin autoantibodies (~55%) and ZnT8 autoantibodies (~50%). In a combined analysis, 94% of Japanese patients with T1D can be defined as having type 1A diabetes. Furthermore, autoantibodies to ZnT8 and IA-2 are associated with childhood-onset and acute-onset patients. Thus, it is important to develop a diagnostic strategy for patients with type 1A diabetes in consideration of the age or mode of disease onset. Keywords: anti-islet autoantibodies, autoimmune thyroid disease, prediction, type 1 diabetes, Zinc transporter 8

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Is diabetes a side effect of immunosuppression?

Martha Walker, DPT, CSCS Chris L. Wells, PhD, PT, CCS, ATC At the time of your organ transplant, you were placed on a regimen of immunosuppressant medications to prevent your immune system from rejecting the donor organ. There are many different immunosuppressant medications you may have been prescribed, including corticosteroids, tacrolimus, cyclosporine, mycophenolate, azathioprine, and sirolimus.

  • These medications are vital for your new organ’s survival; however, many of them come with mild to severe unwanted side effects.
  • But there are steps you can take to lessen their impact.
  • One of the major side effects of corticosteroids is osteoporosis.
  • Osteoporosis is when the density of your bones is decreased, increasing the risk for fractures.

Any bone in your body can be affected; however, fractures are most commonly seen at the hip, spine, or wrist. To learn more about osteoporosis, please go www.apta.org and search under osteoporosis (select the first option followed by selecting “body” which will bring you to a pamphlet on osteoporosis).

  • The effects of osteoporosis can be lessened through exercise, supplemental Vitamin D and calcium, and medications such as Fosomax and Boneva, which you can ask your doctor about.
  • It is important to engage in an exercise program that includes weight bearing activities and resistance training to maintain your bone density, and hopefully make your bones stronger and lessen the risk for fractures.

Weight bearing activities require your bones and muscles to work against gravity and absorb forces from the ground. This can be walking, jogging, stair climbing or dancing. Resistive training, which can include weight training with free weights, machines, or resistive bands, can also improve your muscle strength and therefore bone health particularly for the long thigh bone, femur.

  1. The benefits of resistance training do not end at osteoporosis.
  2. It can also improve your overall strength, balance and reaction time, putting you less at risk for falls.
  3. Several immunosuppressant medications have been linked to a decrease in muscle function.
  4. Tacrolimus and cyclosporine derived medications have been linked to a delay in muscle contraction, decrease in coordination between the different types of muscle fibers to efficiently contract and relax, and a decrease in the adaptability of muscle fibers to change to meet the demands we place upon our muscles.

Corticosteroids also adversely affect muscle fibers, particularly the type two muscle fibers that contract rapidly to produce immediate force or power so we can respond quickly. Corticosteroids decrease muscle protein production and decrease the ability of the muscle to produce muscle energy in an effective manner.

  1. Participating in a general exercise program that includes aerobic and resistive training appears to improve muscle function and decreases the adverse effects on the muscles.
  2. Another side effect of immunosuppressant medications is hyperglycemia (high blood sugar) and secondary diabetes because they may alter the way your body manages glucose (sugar).

It is important to routinely check your blood sugar and work closely with an endocrinologist to establish an effective medication regimen to maintain stable blood sugar level that is close to normal, 80 to 120. Exercise can help lower your blood sugar and possibly decrease medications requirements.

  • Aerobic exercise such as walking, biking and swimming for 30 minutes four-five days a week is very helpful and can lead to an improvement in your health, along with resistive training to increase your muscle mass, which will improve your body’s ability to utilize glucose.
  • Another way to decrease the adverse effects of hyperglycemia or diabetes is to improve your diet.

Most of us need to increase the amount of lean protein (chicken, fish and lean beef), vegetables, and whole grains that we eat. It is also important to limit your consumption of sweets. As with starting any diet and exercise program, it is important to check first with your physician and health care providers to obtain their input and advice.

Types : walking, jogging, biking, swimming, dancing
Duration : 30 minutes
Intensity : moderate level (experiencing shortness of breath but can still talk)
Frequency : 4-5 days a week

Table 2: Resistive Training

Upper Body Lower body
Military Presses: Sitting with good posture, raise your arms over head. Step Ups : Place one foot on a step, press up to transfer your weight onto the step, and then lower down slowly. Avoid using the other leg to push yourself up onto the step.
Shoulder Abduction: Sitting with good posture, raise your arms out to the side until shoulder height. Hip Abduction : Standing with good posture, lift your leg out to the side while keeping your hip and knee straight and your foot pointing straight ahead.
Push Ups: either from the floor or against the wall, lower your straight body to the floor or wall, then press up to straighten your arms. Hip Extension: Standing with good posture, lift your leg backwards while keeping your hip and knee straight, and your upper body still.
Heel Walking : while standing next to your kitchen counter for balance, lift your toes and front of foot off floor. Then walk the length of the counter on your heels.

Last Reviewed: 12/21/2021

What is the most common cause of immunosuppression?

Most commonly, immune suppression happens due to an autoimmune disease, such as lupus, rheumatoid arthritis, or type 1 diabetes. The occurrence of frequent infections with severe symptoms is the primary sign of a suppressed immune system.

Why can the immunosuppressant drug prevent diabetes?

How do immunotherapies work? – Earlier research has shown that ‘immunosuppressant’ drugs (similar to those used after an organ transplant) weaken the immune attack in Type 1 diabetes. This helps to prevent the destruction of insulin-producing beta cells and can lead to short-term improvements in blood glucose control.

  1. But if the whole immune system is weakened, people are more vulnerable to infections and cancer.
  2. So researchers are working to selectively target parts of the immune system thought to be directly responsible for the attack in Type 1 diabetes.
  3. This MonoPepT1De study was designed to see if peptide immunotherapy is safe and to study its effect on the immune system in people with Type 1 diabetes.

During the study, participants were injected with small fragments of proteins that are recognised and attacked by the immune system in Type 1 diabetes. In this way, researchers hope to desensitise the immune system to these specific proteins, slowing down the attack against beta cells.

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