Autoimmune (type 1) diabetes

Research output: Chapter in Book/Report/Conference proceedingBook chapter

Standard

Autoimmune (type 1) diabetes. / Delli, Ahmed; Lernmark, Åke.

The Autoimmune Diseases. ed. / Noel Rose; Ian MacKay. Academic Press, 2013. p. 575-585.

Research output: Chapter in Book/Report/Conference proceedingBook chapter

Harvard

Delli, A & Lernmark, Å 2013, Autoimmune (type 1) diabetes. in N Rose & I MacKay (eds), The Autoimmune Diseases. Academic Press, pp. 575-585.

APA

Delli, A., & Lernmark, Å. (2013). Autoimmune (type 1) diabetes. In N. Rose, & I. MacKay (Eds.), The Autoimmune Diseases (pp. 575-585). Academic Press.

CBE

Delli A, Lernmark Å. 2013. Autoimmune (type 1) diabetes. Rose N, MacKay I, editors. In The Autoimmune Diseases. Academic Press. pp. 575-585.

MLA

Delli, Ahmed and Åke Lernmark "Autoimmune (type 1) diabetes". and Rose, Noel MacKay, Ian (editors). The Autoimmune Diseases. Academic Press. 2013, 575-585.

Vancouver

Delli A, Lernmark Å. Autoimmune (type 1) diabetes. In Rose N, MacKay I, editors, The Autoimmune Diseases. Academic Press. 2013. p. 575-585

Author

Delli, Ahmed ; Lernmark, Åke. / Autoimmune (type 1) diabetes. The Autoimmune Diseases. editor / Noel Rose ; Ian MacKay. Academic Press, 2013. pp. 575-585

RIS

TY - CHAP

T1 - Autoimmune (type 1) diabetes

AU - Delli, Ahmed

AU - Lernmark, Åke

PY - 2013

Y1 - 2013

N2 - Autoimmune (type 1) diabetes (AI-DM) is a multistage disorder. Children are born genetically predisposed to putative environmental exposures. These trigger an aggressive, selective and chronic autoimmune response against the pancreatic islet beta cells. This stage is marked by autoantibodies against insulin, glutamic acid decarboxylase (GAD65), IA-2 and the ZnT8 transporter. Progression to clinical onset of diabetes is highly variable but the time to onset is shortened with an increased number of islet autoantibodies. Both islet autoantibodies and diabetes are associated with HLA-DQ on chromosome 6. More than 50 non-HLA genetic factors, mostly associated with the human immune response also contribute. It remains to be clarified to what extent HLA-DQ and the non-HLA genes contribute to the initiation of the chronic islet autoimmunity, progression to diabetes, or both. Insulin replacement therapy is still the only treatment as all attempts to halt the loss of beta cells by immunosuppression or immune modulation have failed so far.

AB - Autoimmune (type 1) diabetes (AI-DM) is a multistage disorder. Children are born genetically predisposed to putative environmental exposures. These trigger an aggressive, selective and chronic autoimmune response against the pancreatic islet beta cells. This stage is marked by autoantibodies against insulin, glutamic acid decarboxylase (GAD65), IA-2 and the ZnT8 transporter. Progression to clinical onset of diabetes is highly variable but the time to onset is shortened with an increased number of islet autoantibodies. Both islet autoantibodies and diabetes are associated with HLA-DQ on chromosome 6. More than 50 non-HLA genetic factors, mostly associated with the human immune response also contribute. It remains to be clarified to what extent HLA-DQ and the non-HLA genes contribute to the initiation of the chronic islet autoimmunity, progression to diabetes, or both. Insulin replacement therapy is still the only treatment as all attempts to halt the loss of beta cells by immunosuppression or immune modulation have failed so far.

KW - Diabetes

KW - type 1

KW - Autoimmune diabetes

KW - Islet autoimmunity

KW - Islet autoantibodies

KW - Insulitis.

M3 - Book chapter

SN - 0123849292

SP - 575

EP - 585

BT - The Autoimmune Diseases

A2 - Rose, Noel

A2 - MacKay, Ian

PB - Academic Press

ER -