Autoimmune Disease

Autoimmune Disease: Lupus Immune System
By: Sammatha Stiff
TABLE OF CONTENTS
Introduction……………………………………………………………………………………2
Genetics of Autoimmune Disease……………………………………………………………3
Systemic Lupus Erythematosus……………………………………………………………….5
Genetics of Systemic Lupus Erythematosus………………………………………………6
Conclusion………………………………………………………………………………………7
Literature cited…………………………………………………………………………………9

Introduction
Autoimmune disease happens when the immune system turns against itself and attack healthy tissues. Lupus happens when the body immune system start attacking tissues and organs. It starts when autoantibodies start attacking the body. The immune system does not realize which ones are healthy and which ones are not. The immune system usually fights off attacks on the body. The immune system protects the body when it is under attack with viruses. It starts when autoantibodies start attacking the body. The immune system creates antibodies that can protect against bacteria and viruses. When the immune response turns from self-molecules, immune responses cause immunologic tolerance to break down, which comes from autoimmune disease.
However, when immunologic happening from the immune response to self-molecules, therefore becomes unknown. The immune system is supposed to protect the body against invaders with its important parts, such as a set of chemicals and proteins. Antigen comes along because self-molecules and foreigners trigger it. Immune cells are found mainly in organs such as the skin and digestive tract. Immune cells and cell producers come together because of the immune system. When T cells and B lymphocytes join, they present the immunocompetent cells. The T and B lymphocytes play an important role in the immune system because of the nonspecific effectors. Nonspecific effectors response first and quick to defend the body, also known as killer cells. The change in the T cells can come from the immune system coming to age, the aging process comes from thymus involvement. When T cells are decreasing it’s because of the levels of cellular and molecular. T cells doesn’t recognize itself or invading antigen. Autoantibodies have been used to develop an autoimmune response.
Autoimmunity is the immune response of organisms with its own tissues and healthy cells. In order to understand autoimmune disease, it must be considered that the autoimmunity has an immune regulation. Autoantibodies come about from the immune cells that are autoreactive. The autoimmune response moves through the body, and it includes organs and nervous systems. Autoimmunity can come about from genetics and environment. Epigenetics must be involved with autoimmunity because of the nucleotide sequence from DNA. It has histone identification, noncoding RNA, and DNA methylation which plays an important role in epigenetics. The microorganism influences initiation and autoimmune response. Microbiota also was known for microorganism that trigger the induction. While the immune system starts fighting itself, autoimmune disease breakdown the body when the immune system stops working because genetics of autoimmune disease, systemic lupus erythematosus, and genetics of systemic lupus erythematosus.

Genetic of Autoimmune Disease
“Autoimmune diseases occur in up to 3–5% of the general population” CITATION Mar10 l 1033 (Marrick, John, & Kotzin, 2010) .The environment and the host of genes are controlling the autoimmune disease. When the reactive and cells of the immune system are affected because of the susceptibility to autoimmunity because of the environment and a host of genes. The T and B cells holds the antigen and what organs are next to be targeted when the immune attacks. The antigen presentation and recognition usually affect organs and antigen specificity, which cause expression and response to the organ being target. The disease caused by autoimmune usually depends on what organ is targeted base on the immune response. Each organ in the body has a specific autoimmune disease and response to an antigen expression.
The CD4+, CD8+, and T cells have a key responsibility that can conciliate the autoimmune organ damage. When the antigen-specific T cell response, it, therefore, becomes a marker for autoantibodies. When the body is damage it has to used autoantibodies and CD4+ T cells to help. For example, SLE has high levels of antibodies because of the nuclear antigens. The autoimmune disease begins responding to antigen, furthermore would or would not limit to a single organ. The single initiating shows evidence for autoimmune diseases that involves antibodies that turns on antigens.

Autoimmune response by the antigen and organ specificity are controlled by gene expression. Gene expression is defined as a process of information from a gene is in the functional gene product, such as protein. The genes are not the same, therefore it leads to immunoreactivity. Major Histocompatibility Complex which is also called alleles encoding class II major are characteristics of genes. There are different MHC and autoimmune disease have been made countless times. When MHC class II alleles are used with autoimmune disease, it’s because peptides are presented from cells from autoreactive CD4+ T cells. The antigen-specific mature can affect MHC class II. The display and identification of autoantigens are affected by genes that do not involve encoding MHC. These genes influence the expression also hands out molecule in target tissues and organs. The infections and inflammation can be limited with antigen cells. The antigen cells can give approval to inflammation to produced proteins.
Systemic Lupus Erythematosus
Lupus is an autoimmune disease that happens when the immune system starts attacking organs and tissues. It began when autoantibodies start attacking the body. The immune system does not recognize healthy and nonhealthy tissues, but the immune system normally fights off attacks. Systemic Lupus Erythematosus is a chronic disease because it causes inflammation in connective tissues. SLE is considered a copy of systemic autoimmune disease because systemic lupus erythematosus is heterogeneous. Autoantibodies are presented in SLE. The factor of systemic lupus erythematosus can be the environment, hormonal, immunoregulatory, and genetic. The 1q and 6p chromosomes are gathered together because of different genes that cause the expression in SLE. The environment can be ultraviolet light and infections. Hormonal can be from the regulation of genes central.

SLE can multiply and be diverse because of the immune system abnormality. When lymphocyte B overactive meaning if they worked too hard it therefore, becomes accountable for making autoantibodies. Some abnormality and autoantibodies mainly contributed to systemic lupus erythematosus, but other make a disease. T-cells control lymphocytes B, because it provides cognate help. B-cells function is developed because of cytokines 6 and 10. When T-cells are present it decreases the cellular cytotoxic response. Furthermore, that mess with interleukin-2, which cause more infection. Unknown autoantibodies can be put in tissues causing inflammation. It also would cause immune complexes. Nuclear antigens come along and free excess with apoptosis and cells.
The cell singling takes immunocompetent cells through a process for the external antigen. After its finish with the antigen receptor, it moves to B lymphocytes and T cells to generally respond with hyperphosphorylations, which basically is significant. The reaction has a generally low concentration of T cells of CD3 receptors and taken over by proteins. Protein kinase A decrease because of CD3 in a subtle way. It becomes for all intents and purposes involve with phosphorylation of translation initiation, which will cause for it to increase, which essentially is quite significant. When kB is low it usually because of the enhancement for activation of a transcript.

Genetic of Systemic Lupus Erythematosus
The development of SLE comes from genetic factors that are a predisposition. It’s very unusual for SLE to come from one single gene. SLE is more likely to come from many genes. The low number of C4 is the reason for a decrease in self-reactive B cells. The necrotic material was removed because of the low number of C1q. The risk of SLE increase at a high rate when every allele comes together, and several genes are affected. However, SNPs which stands for single nucleotide polymorphisms has been related to SLE because of the noncoding DNA with an immune response. SNPs has been connected to SLE because genes are made that helps abnormal T-cells function in SLE. The connection is TNP1, PRDM1, JAZE1, UHRF1BP1, AND IL10 has been risking factors for SLE. It has been identified that about 15% of the heritability of SLE has loci finding.

The process epigenetic changing like DNA hypomethylation has been another cause for SLE from the environment. Before we move on, epigenetic is the study of change from nongenetic influences on gene expression. The virus usually sets off systemic lupus erythematosus. When Epstein Barr virus-infected and higher viral load because of seroconversion. The comparison between lupus autoantigen RO and EBV antigen while including CD8+ T cells can tell what contribute to SLE. The DNA methylation and histone modifications control the accessibility and gene expression. The gene becomes involved with the pathogenesis of SLE because of hypomethylated.
Systemic Lupus Erythematosus occurs because antigen receptor-mediated becomes connected with T cells. When T cells realize antigen and autoantigen are connecting singular with CD3 and after putting FcR in place after. Once lipid rafts and cholesterol-rich scaffolds are added in the mix it changes the disease expression. The main T cells activation is Interleukin-17 which play a role in immune response for bacteria and fungi. The minute it’s not enough of interleukin-2 some cells began to die. The molecule of CD44 always increases T cells in SLE. The cell usually moves to chemokine because healthy subjects and then organs are damaged. Autoantibodies are increasing because of the tolerance checkpoints.
Conclusion
The information presented in the research would hold important material is about just how autoimmune disease show the immune system began to fight itself. The immune system doesn’t realize which are the body own healthy tissues and which are invaders. The research into the genetics of autoimmune disease shows how genetics and environment play role in the finding of why the immune system fights itself. It breaks down how the immune system functions. If something stops working everything in the immune system began to function wrong. This information also gives details on what goes through a person body who dealing with systemic lupus erythematosus. The genetics of systemic lupus erythematosus show the connection it has with autoimmune disease genetics. This research finding will show that when something stops working in the body it, therefore, throws the body process off.

Literature Cited
BIBLIOGRAPHY Baccala, R. (2017). The multiple pathways to autoimmunity . Nature Immunology, 716-724.

Chao, D., & Yun, D. (2014). Genetics of systemic lupus erythematosus immune response and organ resistance to damage . Current Opinion in Immunology, 87-96.

Curtis, M. (2016). Autoimmune disease: conceptual history and contributations of ocular immunology. Survey of Ophthalmology , 680-688.

Franco, M., & Guzzo, M. (2014). Pain and systemic lupus erythematosus . Reumatisma , 33-38.

Mark, A. (2014). Environmental factors, toxicants and systemic lupus erythematosus . US National Library of Medicine of National Institution of Health , 45-60.

Marrick, P., John, K., & Kotzin, B. L. (2010). Autoimmune disease: why and where it occurs . Nature Medicine , 1-5.

Schmid, R., Grimbacher, B., & Writte, T. (2017). Autoimmunuty and primary immunodefiency: two sides of the same coin. Nature Rhemumatology , 728-732.

Wang, L. (2015). Human autoimmune disease: a comprehensive update. Journal of Internal Medicine , 369-395.