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Review
. 2003 Feb;56(1):1-10.
doi: 10.1136/mp.56.1.1.

Molecular aspects of type 1 diabetes

M A Kelly  1 , M L Rayner, C H Mijovic, A H Barnett
Affiliations
Review

Molecular aspects of type 1 diabetes

M A Kelly et al. Mol Pathol. 2003 Feb.

Abstract

Type 1 diabetes is a T cell mediated autoimmune disease, characterised by the selective destruction of pancreatic beta cells, and susceptibility is determined by a combination of genetic and environmental factors. The environmental agents implicated include viruses and dietary factors, although none has yet been shown to be directly responsible for triggering beta cell autoimmunity. The genetic factors that influence disease risk have been subjected to more intensive study and two gene regions of major importance have been identified: the human leucocyte antigen locus and the insulin gene. This review will focus on the mechanisms by which these genes might influence the risk of developing type 1 diabetes.

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Figures

Figure 1
Figure 1
A simplified map of the major histocompatibility complex on chromosome 6p21, showing the genes arranged in three classes. Hsp, heat shock protein; TNF, tumour necrosis factor.
Figure 2
Figure 2
A diagrammatic representation of (A) a human leucocyte antigen (HLA) class I molecule and (B) an HLA class II molecule, showing the antigen binding clefts.
Figure 3
Figure 3
Antigen presentation to the T cell receptor of a CD4 positive helper T cell by a human leucocyte antigen class II molecule.
Figure 4
Figure 4
The antigen binding cleft of a human leucocyte antigen class II molecule showing the binding pockets (P1, P4, and P9) and the amino acid residues implicated in peptide binding and T cell activation.
Figure 5
Figure 5
The antigen binding cleft of a human leucocyte antigen class II DQ molecule, showing the salt bridge between residues β57 and α79.
See this image and copyright information in PMC

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MeSH terms