Antinuclear Antibody Assessment Essay

ANA: test for these autoantibodies (very general); DsDNA (+): Making antibodies to and attacking own DNA; Anti-Sm (+): these antibodies generally interfere with the cells metabolism and are responsible for the symptoms specifically seen with SLE. Here, they are specifically targeted at smooth muscle. CRP elevated: also indicates presence of inflammation, but is more specific towards disease activity; ESR elevated: indirectly indicates the activity of the disease and presence of inflammation; C3 and C4 (decreased): C3 and C4 usually attack the membranes of viruses and bacteria, but in the case of lupus, they attack the own body’s cells. When C3 and C4 suggest the disease is active

Makover, M. & Zieve, D. (2011, February 14). Systemic Lupus Erythematosus. National Center for Biotechnology Information. Retrieved July

SLE is idiopathic, which means that the cause of the disease is unknown. It is linked to having several factors that can effect it. For example, genetics, environmental factors, and gender and/or hormones. “The disease is not linked to a certain gene, but people with lupus often have family members with other autoimmune conditions. There may be environmental triggers like ultraviolet rays, certain medications, a virus, physical or emotional stress, and trauma. SLE affects more women than men. Women also experience worsening of symptoms during pregnancy and with their menstrual periods. Both of these observations have led some medical professionals to believe that the female hormone estrogen may play a role in causing SLE. However, more research is still needed to prove this theory” (Herndon, n.d.). Our patient’s causes are unknown of why he has Systemic Lupus. We do know through patient history a previous family member does have an autoimmune disease. Also, from his frequent sun exposure he has developed a skin rash on his extremities and face.

To understand autoimmune diseases, the general characteristic of autoimmunity must be addressed. Autoimmunity is defined, in short, as “ misdirected immune response”. A healthy person is equipped with the mechanisms necessary to defend the body from pathogens within the immune system. When autoimmunity is present in an individual, something within the immune system is

Systemic Lupus Erythematosus is a very rare and severe autoimmune disease. While the symptoms vary, lupus commonly affects the skin, joints, and mucous membrane (Brown, Bond, & Waldron, 2014). However, systemic lupus erythematosus (or lupus, for short) can become a multi-organ disease resulting in further complications. Because lupus is so rare and the symptoms vary, diagnosis is difficult and often does not occur until the disease is in its latter stages. However, in the detection of the disease, Brown, Bond, and Waldron (2014) express the importance of noticing certain common symptoms in young females, which are severe fatigue, mouth ulcers, headaches, rashes (especially those caused by the sun), and flitting arthralgasis (joint pain) and

Since rheumatoid arthritis is a systemic disease, it can also affect other organs and tissues, but it primarily attacks the joints in a symmetrical fashion. Rheumatoid arthritis develops from an abnormal immune response caused by exposure to an antigen, in a patient that is genetically susceptible. Autoantibodies develop and attack the patient’s cartilage and synovial tissues once the antigen exposure has occurred (Nelson, 2011). One of the most common

Many SSc patients have increased activated T cells and soluble interleukin-2 (IL-2) receptor [8, 9]. Some SSc patients also have CD25+ CD4+ T cells that are type I collagen (COL1) specific, an ECM protein that is often overexpressed in SSc [10]. Many SSc patients present with autoantibodies. Though the importance of autoantibodies in disease progression is debated, they are useful in predicting subset and disease progression [11]. Common SSc–related autoantibodies include, anti-centromere antibodies (ACA), anti-Scl-70, anti-topoisomerase (TOPO), and anti-nucleolar antibodies including anti-U1-RNP, anti-fibrillarin, anti-RNA polymerase I, II, III, anti-U3-RNP, anti-Th/To, and anti-Pm/Scl. The types of autoantibodies produced are often dependent on SSc subset and ethnicity

A symptom of this autoimmune system disease includes tender and warm, swollen joints, usually in the smaller joints of your body.

Arthritis is a term that is used to describe any disorders that affects the joints, ranging from limited areas, self-limiting conditions, to the systemic immune-mediated processed. The form, severity of the symptoms, and the complexity of the treatments can vary depending on the type of the disease. The various rheumatic conditions share a noticeable or accompanying symptom of the joint inflammation (Porth, 2015, p. 1119).

Hasegawa M. Biomarkers in systemic sclerosis: Their potential to predict clinical courses. Journal of Dermatology. 2016; 43: 29-38.

Due to the irreversible damage that occurs in RA, there is a need to improve the identification and diagnosis of early RA. The primary serological tests for RA used to be assays detecting rheumatoid factor; however, nowadays ACPA assays are being used clinically. The most widely known autoantibody is the rheumatoid factor (RF). These IgM autoantibodies are directed against the Fc portion of IgG molecules. RF can be detected in about 75% of RA patients; however, it is also found in the healthy elderly population (5). Thus, it is not very specific. In addition, false positive RF results occur in patients with chronic infections and other rheumatic and inflammatory

In the world in which we live, autoimmune disorders are becoming more and more widespread, presenting a new epidemic of life-threatening diseases. They are included on the list of ten most common reasons for mortality in children and women up to 64 years of age ("Autoimmune Statistics - AARDA", 2016). According to the National Institute of Health, the estimated number of people suffering from autoimmune-related diseases in the USA alone exceeds 23 million people, and the number keeps growing from year to year. The exact number of autoimmune disorders is unknown due to the fact that the origin of some diseases is not fully understood. At the moment, scientists distinguish approximately 80 autoimmune-related disorders, all of which are considered incurable. Since the nature of autoimmunity is not fully investigated, no cure has been found for any autoimmune diseases so far. Autoimmune conditions may influence any tissues of the body, including skin (psoriasis), limbs (rheumatoid arthritis), endocrine glands (Hashimoto’s disease, type I diabetes) or digestive organs (celiac disease) ("Autoimmune Statistics - AARDA", 2016). Some of the autoimmune disorders exhibit slow disease course with feeble symptoms, while other disorders are manifested rapidly, imposing an immediate threat to patient’s well-being, and, sometimes, to the patient’s life. Lupus is an example of such dangerous autoimmune disorder.

Systemic lupus erythematosus (SLE) cauaes the body to produce antibodies against itself (autoimmune disease), specifically against proteins in the cell nucleus. Self-antigens in the form of nucleosomes, single stranded, double stranded DNA or apoptotic cell bodies are taken up by B cells and DCs and presented to T-Cells through the MHC molecule.

There was a statistically negative correlation between n-Tregs percent and IL10b&IL10LPS, p<0.05. There was a statistically positive correlation between IL10b&IL10LPS and RC, p<0.001, while there was a statistically negative correlation with Hp, p<0.01 and p<0.05 respectively. Conclusion: Although there may be multiple factors that contribute to the induction of warm AIHA, our data indicate that defective suppressive activity of n-Treg cells and IL10/IL12 imbalance could play an essential role in the onset and/or maintenance of this autoimmune disease. Further investigations in 1ry AIHA syndrome in which autoimmunity is a significant feature, holds the promise of identifying new molecular defects that will further elucidate basic mechanisms of self tolerance and provide new targets for therapy.

Since the adoption of ANA as a routine clinical laboratory test, the techniques for their detection and/or measurement have evolved and now encompass a variety of immunological methods [21-30]. IFA using HEp-2 cells is considered the gold standard method for detecting ANA with a number of cons and pros [1-4, 21, 22, 26, 30]. Central to the analytical challenges associated with ANA IFA testing are its labor-intensiveness with significant amount of training required for competence, subjectivity in titer, poor standardization of reagents, and pattern determination, labor-intensiveness as well as a decline workforce in the clinical laboratory [1,-4, 15, 30, 32]. Thus, in some laboratories, ANA IFA has been replaced by high throughput, less subjective methods including ELISA and multiplex assays such as the line immunoassays (LIA) and multiplexed bead assays (MBA) [22-29]. The non-IFA assays differ in source, purity, concentration and binding capacity of the antigens; reference materials or standards used in their development, as well as secondary antibodies (conjugates) detection. Therefore, it is not