An autoimmune disease occurs when the body produces an abnormal immune response against self antigens. It is caused by failure of the tolerance processes to protect the host from the action of self reactive lymphocytes. An organ-specific autoimmune disease involves gradual damage to cellular structures and is replaced by the compensating connective tissue which depletes the function of the gland/organ. Type 1 diabetes (TD1), is an organ specific autoimmune disease characterize by distraction of the B cells located at the islets of langerham in pancreas resulting in a limited secretion of hormone. T1D sufferer’ s immune cells such as anti body T cell and CD8 killer cells mistakenly attacks the B cell as a foreign invader. This mechanism is a results of a delayed hypersensitive response to excessive immune reaction meditated by antigen-activated T lymphocytes, including CD4+ and CD8+ T cytotoxic cell . Mediated hypersensitivity reactions may induced by either environmental and self-antigens. Inappropriate activation these cell mediated cell can be directed against self antigens or exogenous antigens which may cause chronic inflammation in a the islets of pancreas in type 1 diabetes (Lopez 2009, pp. 43). Development of the disease involves both genetic and environmental factors. During development of T1D three major auto-antigens (aAgs), insulin, glutamic acid decarboxylase (GAD) and islet associated antigen (IA-2) are known to be targeted by the human immune system . TD1 is the most common amongst childhood but may manifest at any age. The first factor is the Genetic predisposition in humans, links a strong bond that contribute to disease susceptibility to type 1 diabetes Timmins (2006 pp. 189). Major histocompatibility complex 11 are localize in chromosome 6; in the human leucocyte antigen (HLA) , (which encodes structures responsible for antigen presentation) is associated with the development of type 1 Diabetes. The second factor link to developing type 1 diabetes is the environmental factor that may trigger or accelerate the development of autoimmune disease. A study shown Timmins ( 2006) conducted in mice revealed understanding that virus cells have the ability to induce mediated cell damaging target organs directly or via secretion of inflammatory cytokines that specifically harm beta cells. The relationship of T cell mediated destruction of the beta cell in both mice and human suggests the auto aggressive T cell presence upon the distruption of Beta cell secretion. In humans, a sample gathered from an Autopsy of a recently died T1D patient also provide an insight mechanism of tyoe 1 diabetes as it showed a large infiltration of macrophages and lymphocytes with a high proportion of CD8+ cells in pancreas.
Pathogenesis and Progression
Originate precursor of type 1diabetes originates from both and genetic and environmental factors. In the islets of langerham, of pancreas lies the chromosome 6 HLA class 11; of which abnormal expression of this gene may cause an auto reactive Tcell and CD 8 killer cell activation. In response to this event is the destruction of Beta cell. Upon the islets of langerham cells, the presence of autoantibodies insulin (IAAs), the 65-kDa isoform of GAD (autoantibody to GAD , and the protein tyrosine phosphatase–related molecules IA can be found. These specialized autoantibodies can be use for the traces of clinical type 1 diabetes ( Lopez 2009, pp. 43). The illustrated image below (fig.1.2) is the visual representation of B cell reduced production as the development of type 1 diabetes progress influenced by both genetic and environmental factors.
fig. 1.2 shows the faith of insulin with the reduction of B cell mass. ( Baker et al. 2001,p.3.58-221-229).
Diagnosis and Clinical Symptoms
Genetic (HCL ) chromosome 6 and environment (virus, toxic)
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