ACUTE GRAFT-VERSUS-HOST REACTION IN THE PANCREAS

Publisher Website
Google Scholar
Abstract
Acute graft vs. host reactions (GVHR) were induced in adult (A .times. C57BL/6)F1 hybrid mice by a single i.v. inoculum of A strain lymphoid cells. At periodic intervals, animals were killed, complete autopsies were performed, and the pancreases were examined by light microscopy. Pancreatic immunoreactive insulin and glucagon, plasma glucose and immunoreactive insulin, and urinary glucose and ketones were also monitored. No differences in pancreatic histology, pancreatic immunoreactive insulin, or glucagon, plasma glucose or plasma immunoreactive insulin were recorded between 2 control groups, uninoculated F1 hybrids, and F1 hybrids that had received an inoculum of F1 lymphoid cells. In particular, no lymphocytic infiltrates were identified in the pancreases of control mice. Neither glycosuria nor ketonuria were recorded. In mice experiencing an acute GVHR, the pancreas was the site of multifocal lymphocytic infiltrates which were initially noticed 6 days after induction and became most pronounced 14 days after induction. The infiltrates were centered about vessels, usually veins and venules, major ducts, and ductules rather than about islets. Only those islets adjacent to involved vessels, ducts or ductules were infiltrated by lymphocytes, and then usually at the periphery only. Lymphocytic permeation of the cores of islets was recorded infrequently; most islets remote from sites of vascular and ductular involvement appeared to be normal. No consistent change in pancreatic immunoreactive insulin or glucagon was documented nor did a diabetic-like syndrome develop. Hypoglycemia and hypoinsulinemia were noted and probably reflect general inanition attributable to malabsorption and anorexia in animals experiencing a GVHR. The acute GVHR may not consistently constitute a suitable model for the induction of insulitis or diabetes mellitus. The homing of lymphocytes to pancreatic vessels, ducts and ductules is similar to that observed in the liver and salivary glands in graft vs. host disease. The factors responsible for this characteristic lymphocytic tropism are unknown, but it may be related to the induction of Ia antigens. The consistency and intensity with which the pancreas is infiltrated by lymphocytes in acute GVHR renders this a valuable site in which to isolate and characterize the effector cells in GVHR.