When was it determined that Type 1 Diabetes is an autoimmune disease?

When was it determined that Type 1 Diabetes is an autoimmune disease?

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I just found out today that type 1 diabetes is an autoimmune disease. When was this discovered?

This question has two answers: The difference was first described in 1936 by Harold Percival Himsworth, which described it in this article. At this time it was established that there are two forms of Diabetes, one sensitive to insuline while the other is not. The terms Diabetes type 1 and 2 where established somewhere between 1974 and 1976, for details see the review "The discovery of type 1 Diabetes".

Type 1 diabetes

Type 1 diabetes (T1D), previously known as juvenile diabetes, is an autoimmune disease that is a form of diabetes in which very little or no insulin is produced by the islets of Langerhans (containing beta cells) in the pancreas. [4] Insulin is a hormone required for the cells to use blood sugar for energy and it helps regulate normal glucose levels in the bloodstream. [2] Before treatment this results in high blood sugar levels in the body. [1] The common symptoms are frequent urination, increased thirst, increased hunger, and weight loss. [4] [9] Additional symptoms may include blurry vision, tiredness, and slow wound healing. [2] Symptoms typically develop over a short period of time, often a matter of weeks. [1]

The cause of type 1 diabetes is unknown, [4] but it is believed to involve a combination of genetic and environmental factors. [1] Risk factors include having a family member with the condition. [5] The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas. [2] Diabetes is diagnosed by testing the level of sugar or glycated hemoglobin (HbA1C) in the blood. [5] [7] Type 1 diabetes can be distinguished from type 2 by testing for the presence of autoantibodies. [5]

There is no known way to prevent type 1 diabetes. [4] Treatment with insulin is required for survival. [1] Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump. [10] A diabetic diet and exercise are important parts of management. [2] If left untreated, diabetes can cause many complications. [4] Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma. [5] Long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes. [4] Furthermore, since insulin lowers blood sugar levels, complications may arise from low blood sugar if excessive amount of insulin is taken than necessary. [5]

Type 1 diabetes makes up an estimated 5–10% of all diabetes cases. [8] The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year. [5] Within the United States the number of people affected is estimated at one to three million. [5] [11] Rates of disease vary widely, with approximately one new case per 100,000 per year in East Asia and Latin America and around 30 new cases per 100,000 per year in Scandinavia and Kuwait. [12] [13] It typically begins in children and young adults. [1]

More information on genetics

If you would like to learn more about the genetics of all forms of diabetes, the National Institutes of Health has published The Genetic Landscape of Diabetes . This free online book provides an overview of the current knowledge about the genetics of type 1 and type 2 diabetes, as well other less common forms of diabetes. The book is written for health care professionals and for people with diabetes interested in learning more about the disease.

Type 1 diabetes mellitus as a disease of the β-cell (do not blame the immune system?)

Type 1 diabetes mellitus is believed to result from destruction of the insulin-producing β-cells in pancreatic islets that is mediated by autoimmune mechanisms. The classic view is that autoreactive T cells mistakenly destroy healthy ('innocent') β-cells. We propose an alternative view in which the β-cell is the key contributor to the disease. By their nature and function, β-cells are prone to biosynthetic stress with limited measures for self-defence. β-Cell stress provokes an immune attack that has considerable negative effects on the source of a vital hormone. This view would explain why immunotherapy at best delays progression of type 1 diabetes mellitus and points to opportunities to use therapies that revitalize β-cells, in combination with immune intervention strategies, to reverse the disease. We present the case that dysfunction occurs in both the immune system and β-cells, which provokes further dysfunction, and present the evidence leading to the consensus that islet autoimmunity is an essential component in the pathogenesis of type 1 diabetes mellitus. Next, we build the case for the β-cell as the trigger of an autoimmune response, supported by analogies in cancer and antitumour immunity. Finally, we synthesize a model ('connecting the dots') in which both β-cell stress and islet autoimmunity can be harnessed as targets for intervention strategies.

Conflict of interest statement

The authors declare no competing interests.


Fig. 1. Immunoregulation in health, and immune…

Fig. 1. Immunoregulation in health, and immune dysregulation in cancer, T1DM or immunotherapy.

Type 1 (insulin-dependent) diabetes mellitus: an autoimmune, predictable and preventable disease? Lessons from national registries and new challenges to clinical biology

Type 1 (insulin-dependent) diabetes mellitus is a frequent chronic disease that affects children as well as adults. The disease keeps a life-long burden on patients, their environment and society. Although still incompletely understood, its pathogenesis becomes progressively unravelled. Autoimmune phenomena play an important role, be it as underlying cause or as consequence or innocent bystanders of another primary event. Much of the present knowledge on environmental and genetic triggers for the slow islet beta-cell destruction culminating in clinically overt disease has been acquired through national diabetes registries. The latter represent confidential data- and blood sample banks that collect epidemiological, clinical and biological information from as many new cases as possible within a given area. These registries operate along international guidelines and offer a worldwide framework for optimizing prediction of clinically overt disease in individuals at risk by means of specialized clinical biological tests, carried out in reference laboratories under international quality control surveillance. Better understanding of pathogenesis and predictability of Type 1 diabetes also creates perspectives for disease prevention. Collaborative efforts of national registries provide the methodology of choice to assess the effectiveness of proposed pharmacological or immunological interventions. Several international trials are being contemplated for the near future. Clinical biology will play an important role for selection of the subjects and their further monitoring.

The human gut microbiome in early-onset type 1 diabetes from the TEDDY study

Type 1 diabetes (T1D) is an autoimmune disease that targets pancreatic islet beta cells and incorporates genetic and environmental factors 1 , including complex genetic elements 2 , patient exposures 3 and the gut microbiome 4 . Viral infections 5 and broader gut dysbioses 6 have been identified as potential causes or contributing factors however, human studies have not yet identified microbial compositional or functional triggers that are predictive of islet autoimmunity or T1D. Here we analyse 10,913 metagenomes in stool samples from 783 mostly white, non-Hispanic children. The samples were collected monthly from three months of age until the clinical end point (islet autoimmunity or T1D) in the The Environmental Determinants of Diabetes in the Young (TEDDY) study, to characterize the natural history of the early gut microbiome in connection to islet autoimmunity, T1D diagnosis, and other common early life events such as antibiotic treatments and probiotics. The microbiomes of control children contained more genes that were related to fermentation and the biosynthesis of short-chain fatty acids, but these were not consistently associated with particular taxa across geographically diverse clinical centres, suggesting that microbial factors associated with T1D are taxonomically diffuse but functionally more coherent. When we investigated the broader establishment and development of the infant microbiome, both taxonomic and functional profiles were dynamic and highly individualized, and dominated in the first year of life by one of three largely exclusive Bifidobacterium species (B. bifidum, B. breve or B. longum) or by the phylum Proteobacteria. In particular, the strain-specific carriage of genes for the utilization of human milk oligosaccharide within a subset of B. longum was present specifically in breast-fed infants. These analyses of TEDDY gut metagenomes provide, to our knowledge, the largest and most detailed longitudinal functional profile of the developing gut microbiome in relation to islet autoimmunity, T1D and other early childhood events. Together with existing evidence from human cohorts 7,8 and a T1D mouse model 9 , these data support the protective effects of short-chain fatty acids in early-onset human T1D.

Conflict of interest statement

The authors declare no competing interests.


Fig. 1. More than 10,000 longitudinal gut…

Fig. 1. More than 10,000 longitudinal gut metagenomes from the TEDDY T1D cohort.

Fig. 2. The early gut microbiome is…

Fig. 2. The early gut microbiome is characterized by early heterogeneity of Bifidobacterium species and…

Fig. 3. Consistent changes in enzymatic content…

Fig. 3. Consistent changes in enzymatic content of the gut microbiome in early life.

Fig. 4. Bifidobacterium longum strains are characterized…

Fig. 4. Bifidobacterium longum strains are characterized by HMO gene content and stratified by breastfeeding…

Extended Data Fig. 1. Heterogeneity in early…

Extended Data Fig. 1. Heterogeneity in early taxonomic profiles.

Extended Data Fig. 2. Stability and regional…

Extended Data Fig. 2. Stability and regional differences of taxonomic profiles.

Extended Data Fig. 3. Accrual of microbial…

Extended Data Fig. 3. Accrual of microbial alpha diversity.

Extended Data Fig. 4. Effects of antibiotics.

Extended Data Fig. 4. Effects of antibiotics.

Extended Data Fig. 5. Dynamics of species-specific…

Extended Data Fig. 5. Dynamics of species-specific microbial functional potential during early gut development.

Extended Data Fig. 6. Differences between cases…

Extended Data Fig. 6. Differences between cases and controls.

Extended Data Fig. 7. Contrasting HMO utilization…

Extended Data Fig. 7. Contrasting HMO utilization genes in B. pseudocatenulatum .

Type 1 Diabetes

NIAID is committed to advancing the understanding of autoimmune diseases such as type 1 diabetes and to conducting clinical studies to develop effective prevention and treatment strategies. The following are selected studies supported by NIAID and recruiting people with type 1 diabetes or their relatives. The links lead to full study titles, descriptions, site locations and contact information.

Pathway to Prevention Study (NCT00097292)
The goal of this study is to enhance the understanding of the demographic, immunologic, and metabolic characteristics of individuals at risk for developing type 1 diabetes. Individuals 1 to 45 years old who have an immediate family member with type 1 diabetes (such as a child, parent, or sibling) or individuals 1 to 20 years old who have an extended family member with type 1 diabetes (such as a cousin, niece, nephew, aunt, uncle, grandparent, or half-sibling) may be eligible to volunteer.

Type 1 Diabetes Extension Study (T1DES) (NCT02734277)
The goal of this study is to further the understanding of the immunologic mechanisms underlying maintenance and loss of beta cell function by evaluating the relationship between longitudinal changes in beta cell function and changes over time in biomarkers known to be associated with a response to immune modulating treatments which were used in prior clinical trials. Participants in selected new-onset type 1 diabetes studies conducted by the Immune Tolerance Network may be eligible to volunteer.

Lessons from cancer

The dogma describing T1DM as a disease characterized by total destruction of the insulin-producing β-cells has been shaken by immunohistochemistry studies performed on pancreatic specimens from patients with longstanding T1DM showing the presence of β-cells and insulin microsecretion (C-peptide value of <30 pmol/l) in the majority of these patients, implying that some β-cells resist or escape the immune attack, or that new β-cells are formed 141,142 . The lobularity of this feature (where β-cells in certain pancreatic lobules seem unaffected, while β-cells in other lobules are depleted) might imply formation of new pancreatic lobules with unaffected islets, which increases the sense of urgency to protect β-cells after a diagnosis of T1DM. Confirming these observations, the latest single-cell analysis methods (that is, transcriptomics, mass cytometry and imaging mass spectrometry) have revealed wide heterogeneity in the β-cell population in healthy pancreata but also during disease progression, which might contribute to different sensitivities of β-cells to immune responses 143,144,145,146 . Evidence of this concept is found in multiple sclerosis, where different oligodendrocyte phenotypes have different levels of autoimmune reactions, potentially driving self-destruction 147 . Importantly, while the presence of insulin-positive cells and lack of insulitis in longstanding T1DM might suggest that ‘normal’ islets are present, the lack of detectable C-peptide and differential clustering from islets of non-diabetic donors in multidimensional mass cytometry analyses points to intrinsic differences in patient-derived islets that might reflect prodromal islet distress and prediabetic lesions 145 . Intriguingly, studies of insulin and proinsulin in pancreata from patients with T1DM support the existence of aetiopathological endotypes of T1DM that are associated with age at diagnosis, and point to age-related intrinsic differences in distressed β-cells during insulitis that might lead to different autoimmune reactions 8,50,51 .

A concept is emerging that the immune response seen in T1DM might be one with ‘good intentions’, where the immune response to distressed tissue resembles the immune response that has evolved to detect infected tissue or tumours. Indeed, people carrying T1DM risk gene variants have a hyper-inflammatory immune system 148 . It can be argued that patients with T1DM have an immune system that might be beneficial in patients with cancer. A clear analogy in support of this provocative contention is presented by Lambert–Eaton myasthenic syndrome, which has two different aetiologies: one associated with immune hypersensitivity and autoimmunity (a phenotype shared with T1DM) and one where an antitumour immune response against the voltage-gated calcium channels expressed by small cell lung carcinoma cells and nerve endings causes cross reactivity in the neuromuscular synapse. Patients with small cell lung carcinoma who develop Lambert–Eaton myasthenic syndrome have a better prognosis for cancer survival than patients who do not develop this syndrome 149,150,151 . In addition, in patients with cancer, immune responses that are initiated after antitumour immunotherapy tend to be directed to neoantigens rather than native autoantigens 152 .

In a similar manner to tumour cells that evade immune responses to become more invasive, β-cells have developed active self-protective mechanisms to limit further autoimmune destruction the upregulated expression of inhibitory receptors (such as PDL1) at their cell surface and the increased expression of IDO1 after cytokine challenge illustrate these changes 153,154 . A correlation between loss of IDO1 expression and β-cell destruction extends proof for the participation of these protective mechanisms in the maintenance of the β-cell integrity 155 . In addition, several studies have suggested that increased degranulation and/or a loss of β-cell identity occurs under environmental pressure, which is supported by the defect in insulin production and the presence of polyhormonal cells in the pancreata of patients with T1DM. From these findings, a concept of a ‘β-cell identity crisis’ has emerged where β-cells dedifferentiate into other endocrine cells (α-cells or δ-cells) as a defence mechanism 156,157,158 . Along with this β-cell identity crisis, levels of ‘semi’ β-cells that only express chromogranin A (chromogranin-positive, hormone-negative (CPHN) cells) are increased in the pancreata from patients with T1DM and T2DM and they are scattered throughout the pancreas regardless of inflammation level 158,159 . The origin of these cells is still unknown however, the mere fact that CPHN cells express the autoantigen chromogranin A without this leading to their destruction might suggest that insulin production and the inherent negative molecular effects are needed to drive autoimmunity. Similarly, not all T1DM autoantigens are β-cell-specific chromogranin A and receptor-type tyrosine-protein phosphatase N2 are also expressed in other tissues not affected by an immune attack in patients with T1DM 160 .

By comparing islet and tumour microenvironments, increasing evidence supports the notion that in autoimmune diseases, as in effective tumour immunity or following antitumour immunotherapy, the immune system is acting on dysfunctional cells or tissues that have accumulated aberrant or modified proteins 147 .


Autoimmune diseases present similar symptoms across the more than eighty different types. [6] The appearance and severity of these signs and symptoms depends on the location and type of autoimmune response that occurs. An individual may also have more than one autoimmune disease simultaneously, and display symptoms of multiple diseases. Signs and symptoms presented, and the disease itself, can be influenced by various other factors such as age, hormones, and environmental factors. [7] In general, the common symptoms are: [8]

  • Fatigue
  • Low grade fever
  • General feeling of unwell (malaise)
  • Muscle aches and joint pain
  • Rash on different areas of the skin

The appearance of these signs and symptoms can fluctuate, and when they reappear, it is known as a flare-up. [8] Such signs and symptoms may aid in diagnosis by supporting the results from biologic markers of autoimmune diseases. [9]

There are several areas that are commonly impacted by autoimmune diseases. These areas include: blood vessels, underlying connective tissues, joints and muscles, red blood cells, skin, and endocrine glands (such as thyroid or pancreas glands). [8]

These diseases tend to have characteristic pathological effects that characterize them as an autoimmune disease. Such features include damage to or destruction of tissues where there is an abnormal immune response, altered organ growth, and altered organ function depending on the location of the disease. [8] Some diseases are organ specific and are restricted to affecting certain tissues, while others are systemic diseases that impact many tissues throughout the body. Signs and symptoms may vary depending on which of these categories an individual’s disease falls under. [10]

Cancer Edit

Research suggests an overall correlation between autoimmune diseases and cancer, in that having an autoimmune disease increases the risk or likelihood of developing certain cancers. [11] Autoimmune diseases cause inflammation through a variety of mechanisms, however, the way in which inflammation is created does not greatly influence cancer risk. [11] Rather, the cancer risk is largely dependent on the fact that all autoimmune diseases increase chronic inflammation which has been linked to cancer. [11] Below are some autoimmune diseases most commonly linked to cancer including celiac disease, inflammatory bowel disease (Crohn's disease and ulcerative colitis), multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus. [11]

Following are the few examples of autoimmune diseases. See List of autoimmune diseases for a more exhaustive list.

Coeliac disease Edit

Coeliac disease presents the strongest associations to gastrointestinal and lymphoproliferative cancers. [11] In coeliac disease, the autoimmune reaction is caused by the body’s loss of immune tolerance to ingested gluten, found primarily in wheat, barley, and rye. [11] This explains the increased risk of gastrointestinal cancers, as the gastrointestinal tract includes the esophagus, stomach, small intestine, large intestine, rectum, and anus, all areas that the ingested gluten would traverse in digestion. [11] The incidence of gastrointestinal cancer can be partially reduced or eliminated if a patient removes gluten from their diet. [11] [12] [13] [14] [15] Additionally, celiac disease is correlated with lymphoproliferative cancers. [11]

Inflammatory bowel disease Edit

Inflammatory bowel disease is associated with cancers of the gastrointestinal tract and some lymphoproliferative cancers. [11] Inflammatory bowel disease (IBD) can be further categorized as Crohn's disease or ulcerative colitis. [11] In both cases, individuals with IBD lose immune tolerance for normal bacteria present in the gut microbiome. [11] In this case, the immune system attacks the bacteria and induces chronic inflammation, which has been linked to increased cancer risk. [11]

Multiple sclerosis Edit

Multiple sclerosis is associated with decreased risk of cancer overall but an increased risk of central nervous system cancer, primarily in the brain. [11] Multiple sclerosis is a neurodegenerative disease in which T-cells – a specific type of immune cells – attack the important myelin sheath in brain neurons. [16] This reduces the nervous system function, creating inflammation and subsequent cancer of the brain. [11]

Rheumatoid arthritis Edit

Rheumatoid arthritis presents mild, yet significant associations with focal cancers all throughout the body as well as lymphoproliferative cancers. [11] In rheumatoid arthritis, cells that make up the body’s joints and cartilages become invasive and induce local inflammation. [11] Additionally, the chronic inflammation and over-activation of the immune system creates an environment that favors further malignant transformation of other cells. This can explain the associations to cancer of the lungs and skin as well as the increased risk of other hematologic cancers none of which are directly affected by the inflammation of joints. [17] [18]

Systemic lupus erythematosus Edit

Systemic lupus erythematosus is associated with focal cancers throughout the body and lymphoproliferative cancers. [11] Systemic lupus erythematosus affects multiple organ systems and is characterized by a widespread loss of immune tolerance. [19] The chronic inflammation throughout the entire body promotes the malignant transformation of other cells which contributes to the increased risk of systemic and lymphoproliferative cancers. [11] Conversely, systemic lupus erythematosus is correlated with a decrease in some cancers. This is best explained by increased immunosurveillance in these areas, however, the mechanism for why these areas experience lower incidence is poorly understood. [11]

Aplastic anemia Edit

In aplastic anemia the body fails to produce blood cells in sufficient numbers. Blood cells are produced in the bone marrow by stem cells that reside there. Aplastic anaemia causes a deficiency of all blood cell types: red blood cells, white blood cells, and platelets. [ citation needed ]

The cause is unknown. [3] Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors. [1] There are more than 100 autoimmune diseases. [20] Some common diseases that are generally considered autoimmune include celiac disease, diabetes mellitus type 1, Graves' disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus. [1] [4]

Genetics Edit

Autoimmune diseases are conditions in which the human immune system attacks healthy human tissues within the body. The exact genes responsible for causing each autoimmune disease have not been found. However, several experimental methods such as the genome-wide association scans have been used to identify certain genetic risk variants that may or may not be responsible. [21] Research focusing on both genome scanning and family trait inheritance analysis has enabled scientists to further understand the etiology of autoimmune diseases such as Type 1 diabetes and Rheumatoid arthritis. [22]

  • Type 1 diabetes is a condition in which pancreatic β-cells are targeted and destroyed by the immune system. [23] The condition is a result of neo-natal mutations to the insulin gene (INS) which is responsible for mediating the production of the insulin in the pancreas. [23] The INS gene is located on the short arm of chromosome 11p15.5 in between the genes for tyrosine hydroxylase and insulin-like growth factor II. [24] In addition to chromosome 11, a genetic determinant of type 1 diabetes is a locus called the major histocompatibility complex (MHC) located on chromosome 6p21. [22]
  • Rheumatoid arthritis: Although there is no complete genetic mapping for this condition, several genes are thought to play a role in causing RA. The genes that influence the human immune system contain a TNF receptor associated factor 1(TRAF1). This TRAF1 is located on chromosome 9q33-34. [25] In addition, B1 genes in the human genome contain an increased concentration of HLA-DRB1 alleles that are most commonly seen in RA patients. [26] RA can vary in severity as a consequence of polymorphisms within the genome. [26]

Environmental factors Edit

A range of environmental factors have been recognized as either having a direct role in development, or being a catalyst to many autoimmune diseases. Current studies "indicate" up to seventy percent of autoimmune disease are perhaps due to environmental factors, including: chemicals, infection, diet, and gut dysbiosis. A single set of steps has been identified to be the most likely theory for autoimmune disease onset still there is of yet no definitive proof. [27]

  1. Environmental triggers
  2. Reduced oral tolerance
  3. Gut dysbiosis
  4. Enhanced gut permeability
  5. Increased immune reactivity
  6. Autoimmunity

Chemicals can be found within the direct environment or in the form of drugs, including: hydrazines, hair dyes, trichloroethylene, tartrazines, hazardous wastes, and industrial emissions. [28]

UV radiation is found to be a possible cause of development of the autoimmune disease dermatomyositis, [29] exposure to pesticides plays a role in rheumatoid arthritis development, [30] and vitamin D has been found to be a key in preventing immune dysfunctions in older populations. [31] Infectious agents are considered T cell activators, a step needed for activation of autoimmune diseases. These mechanisms are relatively unknown, but are one of the current alternative theories to explain autoimmune diseases triggered by infection such as Guillain-Barre syndrome and rheumatic fever. [32]

The human immune system typically produces both T cells and B cells that are capable of being reactive with self-protein, but these self-reactive cells are usually either killed prior to becoming active within the immune system, placed into a state of anergy (silently removed from their role within the immune system due to over-activation), or removed from their role within the immune system by regulatory cells. When any one of these mechanisms fail, it is possible to have a reservoir of self-reactive cells that become functional within the immune system. The mechanisms of preventing self-reactive T cells from being created take place through negative selection process within the thymus as the T cell is developing into a mature immune cell. [ citation needed ]

Some infections, such as Campylobacter jejuni, have antigens that are similar (but not identical) to our own self-molecules. In this case, a normal immune response to C. jejuni can result in the production of antibodies that also react to a lesser degree with gangliosides of myelin sheath surrounding peripheral nerves' axons (i.e., Guillain–Barré). A major understanding of the underlying pathophysiology of autoimmune diseases has been the application of genome-wide association scans that have identified a degree of genetic sharing among the autoimmune diseases. [33]

Autoimmunity, on the other hand, is the presence of self-reactive immune response (e.g., auto-antibodies, self-reactive T cells), with or without damage or pathology resulting from it. [34] This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney).

There are so many different theories as to how an autoimmune disease state arises. Some common ones are listed below.

For a disease to be regarded as an autoimmune disease it needs to answer to Witebsky's postulates (first formulated by Ernest Witebsky and colleagues in 1957 and modified in 1994): [35] [36]

  • Direct evidence from transfer of disease-causing antibody or disease-causing T lymphocyte white blood cells
  • Indirect evidence based on reproduction of the autoimmune disease in experimental animals
  • Circumstantial evidence from clinical clues

Symptoms of early autoimmune disease are often the exact same as common illnesses, including: fatigue, fever, malaise, joint pain, and rash. Due to the fact symptoms vary for affected location, disease causing agents, and individuals, it is difficult for proper diagnosis. [37] Typically, diagnosis begins with looking into a patient’s family's history for genetic predisposition. This is combined with various tests, as no single test can identify an autoimmune disease. [28]

Antinuclear antibody Edit

A test used to identify abnormal proteins, known as antinuclear antibodies, produced when the body attacks its own tissues. [37] [28] It may test positive in several disorders. This test is most useful for diagnosing systemic lupus erythematosus, having a 95% positive test rate. [38]

Complete blood count Edit

A test taking measurements on maturity levels, count, and size of blood cells. [28] [37] Targeted cells include: red blood cells, white blood cells, hemoglobin, hematocrit, and platelets. Based on increased or decreased numbers in these counts, underlying medical conditions may be present typically, autoimmune disease is represented by low white blood cell count (Leukopenia). For proper diagnosis, further testing is needed. [39]

Complement Edit

A test used to measure levels of a protein group of the immune system called complement within blood. If complement is found in low levels, this may be an indication of disease. [37] [28]

C reactive protein Edit

C reactive protein, a protein made in the liver generally increases with inflammation, and may be high in autoimmune disease. [37] [28]

Erythrocyte sedimentation rate Edit

This test measures the rate at which a patient’s blood cells descend in a test tube. More rapid descents may indicate inflammation, a common symptom of autoimmune disease. [28] [37]

If these tests are indicative antibody abnormalities and inflammation, further tests will be conducted to identify the autoimmune disease present. [28]

Treatment depends on the type and severity of the condition. The majority of the autoimmune diseases are chronic and there is no definitive cure, but symptoms can be alleviated and controlled with treatment. [8] Overall, the aim of the various treatment methods is to lessen the presented symptoms for relief and manipulate the body’s autoimmune response, while still preserving the ability of the patient to combat diseases that they may encounter. [40] Traditional treatment options may include immunosuppressant drugs to weaken the overall immune response, such as: [41]

  • Non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation
  • Glucocorticoids to reduce inflammation
  • Disease-modifying anti-rheumatic drugs (DMARDs) to decrease the damaging tissue and organ effects of the inflammatory autoimmune response

Other standard treatment methods include: [8]

  • Vitamin or hormone supplements for what the body is lacking due to the disease (insulin, vitamin B12, thyroid hormone, etc.)
  • Blood transfusions if the disease is blood related
  • Physical therapy if the disease impacts bones, joints, or muscles

Because these drugs aim to reduce the immune response against the body’s own tissues, there are side effects of these traditional treatment methods, such as being more vulnerable to infections that can potentially be life threatening. There are new advancements in medicine for the treatment of autoimmune diseases that are currently being researched, developed, and used today, especially when traditional treatment options fail. These methods aim to either block the activation of pathogenic cells in the body, or alter the pathway that suppresses these cells naturally. [40] [42] The goal for these advancements is to have treatment options available that are less toxic to the patient, and have more specific targets. [42] Such options include:

  • Monoclonal antibodies that can be used to block pro-inflammatory cytokines
  • Antigen-specific immunotherapy which allows immune cells to specifically target the abnormal cells that cause autoimmune disease [42]
  • Co-stimulatory blockade that works to block the pathway that leads to the autoimmune response
  • Regulatory T cell therapy that utilizes this special type of T cell to suppress the autoimmune response [40]

The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by Jacobson, et al. They reported US prevalence to be around 9 million, applying prevalence estimates for 24 diseases to a US population of 279 million. [43] Jacobson's work was updated by Hayter & Cook in 2012. [44] This study used Witebsky's postulates, as revised by Rose & Bona, [36] to extend the list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community prevalence, which takes into account the observation that many people have more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females. [44] National Health and Nutrition Examination Surveys conducted in the US from the 1980s to present day, have shown an increase of antinuclear antibodies, a common biomarker for autoimmune diseases. This shows that there has been an increase in the prevalence of autoimmune diseases in recent years pointing to a stronger influence of environment factors as a risk factor for autoimmune diseases. [45]

In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems. In autoimmunity, the patient's immune system is activated against the body's own proteins. In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by cytokines and chemokines, resulting in tissue damage.

Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of inflammatory genes in immune cells is a promising therapeutic approach. [46] [47] [48] There is a body of evidence that once the production of autoantibodies has been initialized, autoantibodies have the capacity to maintain their own production. [49]

Stem cell transplantation is being studied and has shown promising results in certain cases. [50]

Altered glycan theory Edit

According to this theory, the effector function of the immune response is mediated by the glycans (polysaccharides) displayed by the cells and humoral components of the immune system. Individuals with autoimmunity have alterations in their glycosylation profile such that a proinflammatory immune response is favored. It is further hypothesized that individual autoimmune diseases will have unique glycan signatures. [51]

Hygiene hypothesis Edit

According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than in the past, causing their immune systems to become overactive and more likely to misidentify own tissues as foreign, resulting in autoimmune or allergic conditions such as asthma. [52]

Vitamin D Influence on Immune Response Edit

Vitamin D is known as an immune regulator that assists in the adaptive and innate immune response. [53] [54] A deficiency in Vitamin D, from hereditary or environmental influence, can lead to a more inefficient and weaker immune response and seen as a contributing factor to the development of autoimmune diseases. [54] With Vitamin D present, vitamin D response elements (VDRE) are encoded and expressed via pattern recognition receptors (PRR) responses and the genes associated with those responses. [53] The specific DNA target sequence expressed is known as 1,25-(OH)2D3. [53] The expression of 1,25-(OH)2D3 can be induced by Macrophages, Dendritic cells, T-cells, and B-cells. [53] In the presence of 1,25-(OH)2D3, the immune system's production of inflammatory cytokines are suppressed and more tolerogenic regulatory T-cells are expressed. [53] This is due to Vitamin D's influence on cell maturation, specifically T-cells, and their phenotype expression. [53] Lack of 1,25-(OH)2D3 expression can lead to less tolerant regulatory T-cells, larger presentation of antigens to less tolerant T-cells, and increased inflammatory response. [53]

Type 2 diabetes would be considered a(n) . A. immune disorder B. autoimmune disorder C. single-gene disease D. complex disease

The best and most correct answer among the choices provided by your question is the second choice or letter B. Type 2 diabetes is an autoimmune disease.

As a result, your immune system attacks healthy cells. Depending on the type, an autoimmune disease can affect one or many different types of body tissue. It can also cause abnormal organ growth and changes in organ function. There are as many as 80 types of autoimmune diseases.

I hope my answer has come to your help. Thank you for posting your question here in

the answer is c alcoholics anonymous

* endemic (present in a defined area that is a village)

* a bacterial infection (treated with antibiotic)

* communicable by contact (by the hands)

manu-porterage is the most common mode of transmission, it transmits germs from one individual to another via the hands. this concerns infections of exogenous origin.

endemic disease, or endemic disease, refers to a disease that is constantly present in a given population, often tied to a specific geographic origin, as opposed to a pandemic that is not a sporadic disease.

antibiotics are molecules that have the property of killing (bactericidal) or limiting the spread (bacteriostatic) of bacteria.

Watch the video: Βιβλίο: Αυτοάνοσα, Ανοσοποιητικό και Διατροφή 2η Έκδοση (February 2023).