These essays cover all the lecture content of lecture 4 of 6BBBI608. It discusses the pathogenesis of Type 1 Diabetes (T1D).
The first question is: Elaborate on the multifaceted significance of Type 1 Diabetes (T1D), considering its clinical features, epidemiology, and underlying pathology. Subse...
A. Elaborate on the multifaceted significance of Type 1 Diabetes (T1D), considering its clinical
features, epidemiology, and underlying pathology. Subsequently, explain the relevance of
comprehending T1D in an Immunology course, highlighting its classification as an
autoimmune disease and delving into the immunological mechanisms behind pancreatic
beta cell destruction
Type 1 diabetes is an auto-immune disease caused by immune-mediated beta cell destruction
resulting in life-long insulin deficiency. Insulin allows glucose uptake to be used as energy and
to maintain glucose amount in the bloodstream within normal levels. In this essay, we will
elaborate on the multifaceted significance of T1D and explain the relevance of T1d in
immunology.
Symptoms of T1D include hyperphagia, hyperurea and hyperdipsia. The acute complications
of the disease include hyperglycaemia, ketoacidosis and coma whereas the chronic
complications include cardiovascular disease, renal disease and retinopathy. To measure
glycaemic concentration, the HbA1 test can be taken which averages the blood glucose ratio
to the lifespan of a red blood cell. 80% of people with diabetes do no reach the target
concentration, causing significant co-morbidities and excess mortality. T1D has long been
misdiagnosed as a childhood onset disease but most diagnosed individuals are over 30 years
of age. The pathology of T1D includes pseudotrophic islet cells that are small, devoid of beta
cells but retain glucagon and somastatin, as well as insulitis which describes the presence of
immune cells and inflammatory cells within and around the pancreatic islets. Cells include
CD20 B cells, CD3 T cells and alpha cells producing glucagon.
T1D is associated with an increase of pro-inflammatory CD4+ T cells, where more Th1 IFN-
gamma making and Th17 IL-17 making cells are present, with their cytokines directly being.
Toxic to beta cells. Therefore, there is also an increased CD4+ T cell auto-reactivity. Y
Additionally, auto-reactive cytotoxic Lymphocytes target beta cells for destruction in T1D
patients via the recognition of glucose relate pre-pro-insulin epitopes. The IFN-gamma
produced marks the effective function of these CTLs. However, CTL auto-reactivity is common
in non-T1D patients with insulin specific CTLs circulating but not being activated as they are
kept in check by immune regulators. The Tregs dampen the immune reaction safely and
specifically such as iTregs produce the broadly immune regulator cytokine IL-10. Foxp3 Tregs
are not as good immune regulators in T1D patients as they are in non-T1D patients, even
though they are present in the same amounts. In conclusion, the expansion of pro-
inflammatory CD4+ T cells, the increased levels of auto-reactive CTLs and the lower
functionality of immune regulators are markers of T1D.
There is evidence that T1D is an immune disease such as the evident loss of immunological
tolerance to self, clinical responsiveness to immune modulation, transfer of disease by
immune effectors and genetic predispositions. We will delve into each in the following
paragraphs.
Islet cell auto-antibodies (ICAs) demonstrate that beta cells are being killed. This was first
shown by Gian Franco’s experiment where he incubated serum from diabetic patients on
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