NEW YORK (Reuters) -- The ability of a set of immune cells to produce a chemical messenger called interleukin-4 may protect people who are at risk for Type 1 diabetes from developing the disease, according to a study released Wednesday.
Type 1 diabetes, also known as insulin-dependent diabetes mellitus, develops when patients' own immune systems attack the beta cells of the pancreas. But some people with immune systems that appear to put them at risk for autoimmune diabetes never develop the disease. Now, scientists may have discovered what protects them.
Dr. David A. Hafler and colleagues at Brigham and Women's Hospital in Boston, Massachusetts, studied diabetic patients and at-risk individuals without the disease. Included were several sets of identical twins and triplets in which some siblings had diabetes while others did not.
In the January 8th issue of Nature, the researchers report that compared with their healthy siblings, the diabetic siblings had lower levels of a specific subset of immune cells called CD4-CD8-V(alpha)24J(alpha)Q+ T cells. In the diabetics, this subset of T cells secreted only interferon-gamma, while in the healthy subjects, the cells secreted both interferon-gamma and interleukin-4 (IL-4). The investigators add that half of the at-risk subjects who were still healthy had high serum levels of both cytokines.
In a press release, the publishers of Nature point out, "There is some evidence from diabetic mice that IL-4 hinders the development of diabetes, so the failure to produce IL-4 by cells crucial to tissue damage in the pancreas may be, in effect, the removal of the last obstacle to diabetes."
Hafler's team speculates that in people who are predisposed to autoimmune diabetes, these T cells are initially able to produce both cytokines, and the IL-4 helps protect the pancreas from immune system attack.
High levels of IL-4 appear to protect against autoimmune diabetes, say the authors. But the loss of these T cells' capacity to secrete IL-4 may be linked to the development of insulin-dependent diabetes mellitus.
SOURCE: Nature (1998;391:177-181)
