Kuroe K, Yoshihara A, Akiyama M, Takemori H, Yoshida Y
First Department of Internal Medicine, Hirosaki University School of Medicine.
Tohoku J Exp Med. 1993 Jul;170(3):197-205. doi: 10.1620/tjem.170.197.
To elucidate the mechanism of multiple lesions in human primary lymphoma or multiple lymphomatous polyposis of the gastrointestinal tract, we developed a experimental model utilizing mouse hybridoma cells. Syngeneic mice were immunized with human hemoglobin via gastric intubation and a hybridoma clone (13c) between the Peyer's patch cell and mouse myeloma cell was obtained. The 13c cells were infused into normal syngeneic mice through a lateral tail vein. About 2 months after injection mice were sacrificed and their viscera were scrutinized histologically. All 11 mice receiving 13c showed multiple tumors at the colon, microscopic massive invasions at the small intestine, and scattered invasions at Peyer's patch, mesenteric lymph nodes and the spleen, exhibiting the similar distribution patterns as in human multiple lymphomatous polyposis of the gastrointestinal tract. ME-1 or MU-1 cells (hybridomas between P3 and mouse spleen cell) were distributed at the liver, spleen and paraaortic lymph nodes. Such migration patterns of 13c cells and their adherence to vessel walls suggest that multiple invasions may be lymphocyte homing receptor-mediated phenomena.
