Journal of Vaccines & Vaccination

Polyvaccine: Tying up the Loose Ends in the Type 1 Diabetes Chain

Mathhew Steven^* Department of Infectious Disease, University of Copenhagen, Copenhagen, Denmark
^*Correspondence: Mathhew Steven, Department of Infectious Disease, University of Copenhagen, Copenhagen, Denmark, Email:

Received: 01-Jul-2021 Published: 22-Jul-2021, DOI: 10.35248/2157-7560.21.s14.e002

Description

Insulin shortage or insulin resistance, or a combination of the two, are the two main causes of diabetes mellitus. Pancreatitis, pancreatectomy, alcoholic chronic pancreatitis, hemochromatosis, mitochondrial DNA mutations, lipoatrophy, autoimmune disorders, glucagonoma, acromegaly, pheochromocytoma, Cushing's syndrome, and/or medications and poisons can all lead to insulin insufficiency. This is the autoimmune or idiopathic aetiology of type 1 diabetes mellitus (T1DM). Type 2 diabetic mellitus (T2DM) or gestational diabetes can develop from a combination of insulin insufficiency and insulin resistance. T1DM, unlike T2DM, presents acutely with prediabetes as the phase preceding onset, allowing for early management.

T1DM is projected to affect 600,900 children and adolescents under the age of 15 worldwide, with 98,200 children and adolescents of the same age range being diagnosed each year. India has 95,000 children and adolescents under the age of 15 who have T1DM, with a prevalence of 15,900. T1DM problems have a negative impact on patients' quality of life, and even with a thorough diagnosis, it can lead to death in countries with inadequate health services. The cost of medical treatment for T1DM is quite considerable.

The Human Leukocyte Antigen (HLA) class II DRB1-DQA1- DQB1 genotypes are well-known as strong genetic risk factors for T1DM; however, a number of additional genes, divided into the areas of insulin expression, immunological function, and cell function, also play a role. HLA class I alleles, in addition to HLA class II alleles, are linked to T1DM. The extracellular matrix (ECM) is important in T1DM. In the extended vascular ductal pole adjacent to the actual islet, there exist ECM abnormalities.

During the foetal development phase, as well as during postnatal periods, the vascular-ductal pole is implicated in the production of islets. EMC is damaged by myeloid cells that concentrate in insulitis. The formation of normal islets is aided by macrophages and myeloid cells. As a result of the anomalies in the ECM, aberrant islets develop, leading to T1DM. Individual factor management could be aided by a single target vaccine. T1DM, on the other hand, has a number of aims. As a result, combining all feasible vaccinations against the above-mentioned targets, as well as sophisticated gadgets and improved medicines, would help to alleviate the severe load of T1DM. These vaccines can be studied in animal models in accordance with vaccine development guidelines.

Conclusion

T1DM is an autoimmune illness in which a variety of variables have a role in its onset and progression. The global increase in the incidence and prevalence of T1DM, along with the lack of a permanent cure, necessitates the identification of etiological variables and the development of prevention strategies. Many etiological targets have been identified, and it is now thought that immunization against certain viruses and bacteria may be effective in preventing it. T1DM could also be controlled by developing vaccines against a variety of different targets, such as bovine serum albumin and autoantigens. Immune system modulation and immunization against T1DM autoantigens can both help to lessen the disease's incidence and, eventually, to eradicate it completely. After conducting preclinical and clinical trials, a combination of vaccinations against all possible targets can be used to lessen the severe burden of T1DM and eventually put a stop to it.