Immunity and Disease

Question: Write a report on Immunity and Disease. Answer: Research Strategies for Type 1 Diabetes: The strategic research of the Type I diabetes is important to serve the research opportunities and the research progress, prevention, treatment, and future plans related to the type I diabetes. Present researches on diabetes type I are the autoimmune disease applied in mice, which shows a progressive mechanism; where the beta cells of pancreas undergo an irregular process including the insulitis causing inflammation (Saunders et al. 2007). Research progress: This process includes majorly a principle, known as the Hygiene Hypothesis. This principle is classified into the Helminth Infections and the Autoimmunity. The Helminth Infection includes the IL-4, IL-5, IL-13 (comprising the Th2 cells), whereas the autoimmunity includes IL-12, IL-23 (specifically including the Th1 cells and the Th17 cells) (Alvarado et al. 2015). The research strategy on the diabetes type I includes the therapeutic applications of the two types of principles. Helminth infections: Inflammatory Bowel Disease; Multiple Sclerosis. Murine- Type I diabetes; Rheumatoid Arthritis; and Multiple Sclerosis, etc. in human (Herold et al. 2013). In Type 1 Diabetes includes the process in which the mechanism persists in two parts namely, the pancreatic lymph node and the pancreas itself. The antigen presenting cells or the APC consisting with two receptors such as the MHC and the immune receptor (Wilson et al. 2004). The helper T cells bind to the receptor of th e APC with the help of the TCR especially the CD3. The resulting mechanism includes the formation of: 1) Cytotoxic T cells, 2) activated macrophages, resulting in the rupture of the pancreas beta cells. As a result, the situation undergoes diabetes, type I. The type I diabetes potentially destroys the own insulin-producing beta cells, but there are clues to produce the treatments and restoring the cell population (Wilson et al. 2010). Method: The research that would be conducted under the quantitative method. According to the methodology sampling will be conducted with about 50 samples approximately, with 30ml volume of the samples. The sampling includes, blood, and urine for example. These samples would be subjected to random selection and testing. The next step includes the isolation and identification of the diabetic responsible gene with the blood samples. These genes were then be incorporated in mice. The selection of mice should be in such a way that the mice have the eligibility and physical maturation for giving offspring. The genes were incorporated in some stipulated ways: 1) Target gene being radio labelled. 2) and normal gene without the target effects. The mice were taken as females and males. Three sets of couple mice were experimented. The conditions include: 1) with one radio labelled target gene and one normal gene, 2) both the radio labelled target genes, 3) both the normal genes. The stipulated time were given to the experimented mice to mate and produce offspring. This process has been carried out for three times for trial and error method. The resultant offspring with definite results are to me observed and sequenced deliberately. The offspring also could denote the transferring rate of the target gene to the offspring and increase and decrease of the desired disease in the future generations too. Therefore site directed mutagenesis was to be performed for the trial of removing the target diseased gene from the mice itself. The resulting data would be analyzed with statistical analysis in the mean median mode. The mean median mode includes the identification of the average of the testing results of the samples. The respective results are subjected to tabular and a graphical format for the identification of the accumulation of the reports. The percentage of the sample with type I diabetes gene may be subjected to treatment and therapy. These sequences were to undergo such processes like transduction and transcription for the formation of the protein which has been purified from the target diseased genes. These proteins can be incorporated into the desired patients which could help then to gradually remove the diseased gene from the body with mutations and other genetically manipulations. If this treatment and strategy does not work and fails, then similar purification treatment can be done with other sets of patients with the same disease and with other types of sample, where the acquiring of the genomic matter should b more potent. Other, it also be tested for the purification of the insulin itself and be incorporated in the experimental mice to carry on the purification process. (Finlay et al. 2016). Preventions: One of the important factors that should be avoided such as: Hypoglycemia, Hypoglycemia unawareness, and hyperglycemia, etc. Primary preventions includes by preventing the risk factors of the disease. The secondary preventive measure includes the prevention of development of the disease. The tertiary factor includes preventing the complications from the early stages of the disease, early diagnosis, and treatment for the disease (Alvarado et al. 2015). Treatments: This disease is researched to be regulated. Therefore, the research strategy includes the modification of the therapeutic applications and the new researches in type I diabetes. The remedies of the therapeutic methods to resolve the problem of type I diabetes includes: 1) Pancreas transplantation- artificial insulin will no longer be provided to the patient. The patient may include lifetime potent immune-suppressing new insulin producing cells. Although this process may undergo problems and the body may undergo a rejection by the body. 3) Stem cell transplantation- the patients with newly detected type I diabetes may undergo stem cell transplantation (Maizels 2016). 2) Islet cell transplantation- it is of a researched value that the transplanting the involved in the life-threatening disease "type 1 diabetes", are: replacements of the lifelong insulin injections or pumps; monitoring the blood glucose level; maintain healthy diet (Magnuson et al. 2015). Future plans: The future plans for researches on type I diabetes include how the proposals of the research involve in the development of the heath of the people at the risk of diabetes. Therefore based on the present proposals and knowledge of autoimmunity, new approaches for the type I diabetes should be focused mostly in prevention and treatment. Secondly on the basis of the beta cells treatment the research goals should be set to play a crucial role in treatment in all forms of diabetes (Wilson et al. 2010). References: Alvarado, R., OBrien, B., Tanaka, A., Dalton, J.P. and Donnelly, S., 2015. A parasitic helminth-derived peptide that targets the macrophage lysosome is a novel therapeutic option for autoimmune disease. Immunobiology, 220(2), pp.262-269. Finlay, C.M., Stefanska, A.M., Walsh, K.P., Kelly, P.J., Boon, L., Lavelle, E.C., Walsh, P.T. and Mills, K.H., 2016. Helminth Products Protect against Autoimmunity via Innate Type 2 Cytokines IL-5 and IL-33, Which Promote Eosinophilia. The Journal of Immunology, 196(2), pp.703-714. Magnuson, A.M., Thurber, G.M., Kohler, R.H., Weissleder, R., Mathis, D. and Benoist, C., 2015. Population dynamics of islet-infiltrating cells in autoimmune diabetes. Proceedings of the National Academy of Sciences, 112(5), pp.1511-1516. Maizels, R.M., 2016. Parasitic helminth infections and the control of human allergic and autoimmune disorders. Clinical Microbiology and Infection. Saunders, K.A., Raine, T., Cooke, A. and Lawrence, C.E., 2007. Inhibition of autoimmune type 1 diabetes by gastrointestinal helminth infection. Infection and immunity, 75(1), pp.397-407. Wilson, M.S. and Maizels, R.M., 2004. Regulation of allergy and autoimmunity in helminth infection. Clinical reviews in allergy immunology,26(1), pp.35-50. Wilson, M.S., Taylor, M.D., O'Gorman, M.T., Balic, A., Barr, T.A., Filbey, K., Anderton, S.M. and Maizels, R.M., 2010. Helminthà ¢Ã¢â€š ¬Ã‚ induced CD19+ CD23hi B cells modulate experimental allergic and autoimmune inflammation.European journal of immunology, 40(6), pp.1682-1696.