Diabetes Type 1 Immunology Mechanism
Basic Mechanism
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
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
References: Baker, R.L., Mallevaey, T., Gapin, L. & Haskins, K. 2012, "T cells interact with T cells via CD40-CD154 to promote autoimmunity in type 1 diabetes", European journal of immunology, vol. 42, no. 3, pp. 672-689. Fox, C., Kilvert, A. & Sonsken, P. 2008, Type 1 Diabetes, Ebsco Publishing, Ipswich Gan, M.J., Albanese-O 'Neill, A Kolb, H. 1999, "Pathophysiology of type 1 diabetes mellitus", EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, vol. 107, pp. S88-S88. Lopez, J.C. 2010, "Protecting the pancreas.(AUTOIMMUNITY)(type 1 diabetes)(Brief article)", Nature Medicine, vol. 16, no. 1, pp. 43. Todd, J.A. 2009, "Stem cells and a cure for type 1 diabetes?", Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 37, pp. 15523-15524. Todd, J. 1990, "GENETIC-CONTROL OF AUTOIMMUNITY IN TYPE-1 DIABETES", IMMUNOLOGY TODAY, vol. 11, no. 4, pp. 122-129. Tsui, H., Razavi, R., Chan, Y., Yantha, J. & Dosch, H. 2007, " 'Sensing ' autoimmunity in type 1 diabetes", Trends in molecular medicine, vol. 13, no. 10, pp. 405-413.