The role of graft-resident Kupffer cells and lymphocytes of donor type during the time course after liver transplantation?a clinico-pathological study

The liver is thought to be an immunologically privileged organ in the response to inoculated antigens. We previously demonstrated that it is possible to localize inoculated antigens to the liver alone or only to extrahepatic tissue using orthotopic syngeneic liver transplantation (OSLT). In this study, we analyzed more detailed mechanisms of the anti-alloimmune response in the liver. DA rat spleen cells were systemically injected into WS rats (donor spleen cell inoculation, DSI). In the sensitized liver-grafted (SLG) group, after DSI, liver grafts were retrieved from sensitized WS rats, then transplanted into naive WS rats. In the sensitized liver-removed (SLR) group, after DSI, WS rats were totally hepatectomized and given livers transplanted from naive WS rats. All the rats were challenged with heterotopic heart grafts 10 days after DSI. Mean heart graft survival in the control, DSI, SLG, and SLR groups were 11.6 ± 1.6, 10.7 ±2.4, 4.4 ± 1.0, and 24.6 ± 6.3 days, respectively. Accelerated rejection in the SLG group as well as graft prolongation in the SLR group disappeared when OSLT was performed 2 days after DSI or later. Irradiation of DA splenocytes before inoculation did not alter graft survival in SLG. However, pretreatment with gadolinium chloride prior to DSI attenuated the antidonor response in the SLG group. In conclusion, a vigorous antidonor response occurred in the liver after systemic inoculation of spleen cells. It peaked 1 day after DSI and disappeared rapidly. Kupffer cells seemed to play an important role in this phenomenon.

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Role of Kupffer Cells in the Induction of Tolerance after Liver Transplantation

Journal of Surgical Research ◽

10.1006/jsre.1996.0288 ◽

1996 ◽

Vol 63 (2) ◽

pp. 433-438 ◽

Cited By ~ 38

Author(s):

Koichi Sato ◽

Kiyotaka Yabuki ◽

Takanori Haba ◽

Takeo Maekawa

Keyword(s):

Liver Transplantation ◽

Kupffer Cells ◽

Induction Of Tolerance

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A role of Helicobacter pylori infection in the development of duodenal ulcer affer adulf living-related liver transplantation

Gastroenterology ◽

10.1016/s0016-5085(01)81217-8 ◽

2001 ◽

Vol 120 (5) ◽

pp. A246-A246

Author(s):

Y HOSOTANI ◽

C KAWANAMI ◽

M TOJO ◽

T ITO ◽

K OKAZAKI ◽

...

Keyword(s):

Liver Transplantation ◽

Duodenal Ulcer ◽

Helicobacter Pylori ◽

Helicobacter Pylori Infection ◽

Living Related Liver Transplantation ◽

Living Related

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Collagen-Induced Platelet Aggregation: -Evidence Against the Essential Role of Platelet Adenosine Diphosphate

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657015 ◽

1979 ◽

Vol 42 (04) ◽

pp. 1193-1206 ◽

Cited By ~ 9

Author(s):

Barbara Nunn

Keyword(s):

Platelet Aggregation ◽

Time Course ◽

Essential Role ◽

Atp Release ◽

Adenosine Diphosphate ◽

Human Platelets ◽

High Doses ◽

Induced Aggregation

SummaryThe hypothesis that platelet ADP is responsible for collagen-induced aggregation has been re-examined. It was found that the concentration of ADP obtaining in human PRP at the onset of aggregation was not sufficient to account for that aggregation. Furthermore, the time-course of collagen-induced release in human PRP was the same as that in sheep PRP where ADP does not cause release. These findings are not consistent with claims that ADP alone perpetuates a collagen-initiated release-aggregation-release sequence. The effects of high doses of collagen, which released 4-5 μM ADP, were not inhibited by 500 pM adenosine, a concentration that greatly reduced the effect of 300 μM ADP. Collagen caused aggregation in ADP-refractory PRP and in platelet suspensions unresponsive to 1 mM ADP. Thus human platelets can aggregate in response to collagen under circumstances in which they cannot respond to ADP. Apyrase inhibited aggregation and ATP release in platelet suspensions but not in human PRP. Evidence is presented that the means currently used to examine the role of ADP in aggregation require investigation.

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