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. 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. antinuclear antibody a test used to identify abnormal proteins, known as antinuclear antibodies, produced when the body attacks its own tissues. it may test positive in several disorders. this test is most useful for diagnosing systemic lupus erythematosus, having a 95% positive test rate. complete blood count a test taking measurements on maturity levels, count, and size of blood cells. 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. complement 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. c-reactive protein c-reactive protein, a protein made in the liver, generally increases with inflammation, and may be high in autoimmune disease. erythrocyte sedimentation rate 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. if these tests are indicative antibody abnormalities and inflammation, further tests will be conducted to identify the autoimmune disease present. treatment 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. standard treatment methods include: 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 traditional treatment options include immunosuppressant drugs to reduce the immune response against the body's own tissues, such as: 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 because immunosuppressants weaken the overall immune response, relief of symptoms must be balanced with preserving the patient's ability to combat infections, which could potentially be life-threatening. non-traditional treatments are being researched, developed, and used, especially when traditional treatments fail. these methods aim to either block the activation of pathogenic cells in the body, or alter the pathway that suppresses these cells naturally. these treatments aim to be less toxic to the patient and have more specific targets. 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 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 epidemiology 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. jacobson's work was updated by hayter & cook in 2012. this study used witebsky's postulates, as revised by rose & bona, 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. 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. research 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. there is a body of evidence that once the production of autoantibodies has been initialized, autoantibodies have the capacity to maintain their own production. stem-cell therapy main article: stem-cell therapy stem cell transplantation is being studied and has shown promising results in certain cases. medical trials to replace the pancreatic β cells that are destroyed in type 1 diabetes are in progress. altered glycan theory 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. hygiene hypothesis 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. vitamin d influence on immune response vitamin d is known as an immune regulator that assists in the adaptive and innate immune response. 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. 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. the specific dna target sequence expressed is known as 1,25-(oh)2d3. the expression of 1,25-(oh)2d3 can be induced by macrophages, dendritic cells, t-cells, and b-cells. 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. this is due to vitamin d's influence on cell maturation, specifically t-cells, and their phenotype expression. 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.