• Corpus ID: 46910917

A study on the role of genes of innate immunity in type 1 diabetes

  title={A study on the role of genes of innate immunity in type 1 diabetes},
  author={Saikiran K. Sedimbi},
Type 1 diabetes (T1D) is caused by autoimmune destruction of insulin-producing pancreatic β-cells. It is a polygenic disease in which maximal genetic susceptibility is conferred by the presence of MHC class II genes. Circulating autoantibodies against islet cell antigens and mononuclear cell infiltrates, especially CD4 + and CD8 + T cells, are characteristic of the disease. Recent evidence suggests innate immunity may be involved in the disease pathogenesis. The aim of this thesis is to… 


Genes Influencing Innate and Acquired Immunity in Type 1 Diabetes and Latent Autoimmune Diabetes in Adults
  • C. Sanjeevi
  • Biology, Medicine
    Annals of the New York Academy of Sciences
  • 2006
The results from MICA and KIR studies suggest that polymorphism of these genes of the innate immune system identify possible defects in the first line of antiviral defense in the etiology of T1DM.
Predominance of the Group A Killer Ig‐Like Receptor Haplotypes in Korean Patients With T1D
T1D, at least in Koreans, is associated with KIR genes, especially in the group A KIR haplotypes, and there is a close relationship between innate and adaptive immunity.
The role of T-cells in the pathogenesis of Type 1 diabetes: From cause to cure
  • B. Roep
  • Biology, Medicine
  • 2003
The challenge for the future is to determine which factors contribute to the loss of tolerance to beta-cell antigens, and to define what measures T- cells can provide to suppress autoreactivity, since it is becoming increasingly evident that T-cells provide a two-edged sword.
Different KIRs Confer Susceptibility and Protection to Adults with Latent Autoimmune Diabetes in Latvian and Asian Indian Populations
It is concluded that KIRs are important in conferring susceptibility (or protection) to adult patients with LADA in both the authors' study populations, however the KIR genes (and their HLA‐C ligands) conferting susceptibility or protection in these two populations differ, showing a role of ethnicity in disease susceptibility.
Killer Cell Immunoglobulin‐like Receptor Genes in Latvian Patients with Type 1 Diabetes Mellitus and Healthy Controls
It is suggested that a balance between innate and acquired immunity is important, and an imbalance coud lead to T1DM.
Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease
Genes and mechanisms involved in common complex diseases, such as the autoimmune disorders that affect approximately 5% of the population, remain obscure. Here we identify polymorphisms of the
A comprehensive guide to antibody and T-cell responses in type 1 diabetes.
A review of beta-cell antigens, accompanied by their T-cell epitopes, where known, and a discussion of the current understanding of why particular self-proteins become disease-inciting antIGens are presented.
New antigenic targets in type 1 diabetes
Functional studies of the transporter will be key to understanding the role of ZnT8 in type 2 diabetes and measurement of autoantibodies to ZNT8 takes us a step closer to detection of prediabetes in the general population.
The effect of HLA class II, insulin and CTLA4 gene regions on the development of humoral beta cell autoimmunity
The INS and the DRB1 loci appear to contribute to the pathogenesis of type 1 diabetes by initiating/modifying insulin-specific autoimmunity in young children, in whom the appearance of GADA and IA–2A is linked to IAA.
Insulin gene VNTR, CTLA-4 +49A/G and HLA-DQB1 alleles distinguish latent autoimmune diabetes in adults from type 1 diabetes and from type 2 diabetes group.
There was an increased association between LADA and CTLA-4 diabetes-susceptibility genotypes and decreased association with INS VNTR and high-risk HLA-DQB1 alleles, compared with T1D, and the study suggested the need for further investigation into the genetic background and functional genomics of LADA in comparison with T 1D and T2D.