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Clin Immunol. 2015 Feb;156(2):109-18. doi: 10.1016/j.clim.2014.11.007. Epub 2014 Dec 5.

Novel diagnostic and therapeutic approaches for autoimmune diabetes--a prime time to treat insulitis as a disease.

Author information

1
Molecular Development of the Immune System Section, Laboratory of Immunology, NIAID Clinical Genomics Program, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: juhapetrikristian.gronholm@nih.gov.
2
Molecular Development of the Immune System Section, Laboratory of Immunology, NIAID Clinical Genomics Program, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: lenardo@nih.gov.

Abstract

Type 1 diabetes is a progressive autoimmune disease with no curative treatment, making prevention critical. At the time of diagnosis, a majority of the insulin secreting β-cells have already been destroyed. Insulitis, lymphocytic infiltration to the pancreatic islets, is believed to begin months to years before the clinical symptoms of insulin deficiency appear. Insulitis should be treated as its own disease, for it is a known precursor to autoimmune diabetes. Because it is difficult to detect insulitic cellular infiltrates noninvasively, considerable interest has been focused on the levels of islet autoantibodies in blood as measurable diagnostic markers for islet autoimmunity. The traditional islet autoantibody detection assays have many limitations. New electrochemiluminescence-based autoantibody detection assays have the potential to overcome these challenges and they offer promising, cost-effective screening tools in identifying high-risk individuals for trials of preventive interventions. Here, we outline diagnostic and therapeutic strategies to overcome pancreatic β-cell destroying insulitis.

KEYWORDS:

Autoantibody; Insulitis; Tolerance; Type 1 diabetes

PMID:
25486604
PMCID:
PMC4336608
DOI:
10.1016/j.clim.2014.11.007
[Indexed for MEDLINE]
Free PMC Article

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