LOCALIZATION OF LAK CELLS AND IL-2-STIMULATED REGIONAL LYMPH-NODE LYMPHOCYTES BY REGIONAL ARTERIAL INFUSION IN RENAL TUMOR-BEARING RATS

Citation
M. Hayakawa et al., LOCALIZATION OF LAK CELLS AND IL-2-STIMULATED REGIONAL LYMPH-NODE LYMPHOCYTES BY REGIONAL ARTERIAL INFUSION IN RENAL TUMOR-BEARING RATS, Urologia internationalis, 50(4), 1993, pp. 185-191
Citations number
NO
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00421138
Volume
50
Issue
4
Year of publication
1993
Pages
185 - 191
Database
ISI
SICI code
0042-1138(1993)50:4<185:LOLCAI>2.0.ZU;2-L
Abstract
We describe the results of a traffic assay of the regional arterial ad ministration of either lymphokine-activated killer cells or recombinan t interleukin-2-activated regional lymph node lymphocytes in tumor-bea ring rats in comparison with the results of systemic or intracardiac a dministration. The lymphocytes were labeled with Cr-51 before infusion . The distribution and localization of these cells were serially evalu ated by counting the radioactivity of the removed tissues. Concerning arterial administration, the labeled cells were directly infused into the abdominal aorta just proximal to the left renal artery. In the sys temic or intracardiac route, the labeled cells preferentially localize d to the lung, spleen and liver 2 h after injection. Radioactivity of the lung decreased thereafter and that of the spleen increased. In con trast, regional arterial administration yielded a remarkable accumulat ion of radioactivity in the left renal parenchyma 2 and 6 h after inje ction. similar to other distal organs tested. In the renal tumor model , the percentage radioactivity of the tumor tissue (% injectate recove red/g tissue) obtained at 6 h after injection in the arterial administ ration group ranged from 0.40 to 1.33, which was significantly higher (p < 0.05) than that in the systemic administration group. However, th e radioactivity rapidly decreased from the tumor tissue 18 h after the injection. This study raises the essential issue on the mechanism of tumor destruction by lymphokine-activated killer lymphocytes in adopti ve immunotherapy.