Transgenic mice with I-A on islet cells are normoglycemic but immunologically intolerant.

Insulin-dependent diabetes mellitus (IDDM) is caused by a specific loss of the insulin-producing beta cells from pancreatic Langerhans islets. It has been proposed that aberrant expression of major histocompatibility complex (MHC) class II molecules on these cells could be a triggering factor for their autoimmune destruction. This proposal was tested in transgenic mice that express allogeneic or syngeneic class II molecules on the surface of islet cells at a level comparable with that normally found on resting B lymphocytes. These animals do not develop diabetes, nor is lymphocyte infiltration of the islets observed. This immunological inactivity does not result from tolerance to the "foreign" class II molecules.

Anti-islet cell antibodies from NOD mice.

We produced a panel of monoclonal autoantibodies from the spleen cells of prediabetic nonobese diabetic mice. The antibodies were selected on the basis of their ability to bind to the surface of nondiabetic mouse islet cells, and from greater than 4000 hybridomas screened, 35 islet-reactive antibodies were isolated. Most of these reagents also bind to nondiabetic rat and human islet cells and beta-cell tumor lines. A few of the antibodies were found to be reactive with insulin. When tested for cross-reactivity with other cell types, most of the antibodies were found to be islet specific.

Effects of growth temperature on the ingestion and killing of clinical isolates of Listeria monocytogenes by human neutrophils.

In this study, we compared three human isolates (F5380, Scott A, and Murray B) and one laboratory strain (EGD) of Listeria monocytogenes for their resistance to ingestion and killing by human neutrophils. We observed no substantial difference in killing among these strains when they were grown at 37 degrees C. Because it is likely that listerial growth occurs at lower temperatures during food-borne outbreaks of listeriosis, we also compared these strains after they were grown at 22 and 4 degrees C. A general reduction in the ability of human neutrophils to kill L. monocytogenes was observed as the temperature at which the listeriae were grown decreased. Growth at 4 degrees C significantly decreased the killing of all four strains of L. monocytogenes by human neutrophils; two strains (EGD and F5380) were more resistant to killing than were the other two strains (Scott A and Murray B). No obvious relationship was noted between the chemiluminescence response of neutrophils to opsonized listeriae and the ability of the neutrophils to kill listeriae in vitro. Growth at 4 degrees C, however, significantly increased the resistance of L. monocytogenes to killing by hydrogen peroxide.