1996 Fiscal Year Final Research Report Summary
STRATEGY TO CONTROL XENOGRAFT REJECTION,AND POTENTIAL BENEFITS TO APPLY MHC-DEFICIENT DONOR
| Project/Area Number |
06671184
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Chiba University |
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Principal Investigator |
OCHIAI Takenori Chiba University, Department of Surgery, associate proffessor, 医学部, 助教授 (80114255)
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| Co-Investigator(Kenkyū-buntansha) |
KOMORI Akiyoshi Chiba University Hospital, Instractor, 医学部・附属病院, 医員
ISONO Kaichi Chiba University, Department of Surgery, proffessor, 医学部, 教授 (70009489)
GUNJI Yoshio Chiba University, Department of Surgery, assistant, 医学部, 助手 (60241957)
NAKAJIMA Kazuaki Chiba University, Department of Surgery, assistant, 医学部, 助手 (20261919)
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| Project Period (FY) |
1994 – 1996
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| Keywords | leukotrien B4 / MHC / xenograft / FK506 |
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| Research Abstract |
Treatment with leukotrien B4 (LTB4) antagonist (50mg/kg) alone failed to prolong allograft survival, and combination of LTB4 antagonist and FK506 (0.32mg/kg) did not work in allograft model. Mouse skin graft on rats treated with LTB4 antagonist survived 11.5days, while xenograft on untreated rats were reiected in 8 days. Combination of LTB4 antagonist and suboptimal dose of FK brought 14.5 day-graft survival, while MST of FK alone group was 9.5 days. In the CML analysis, pig-effectors stimulated with B10.BR (H-2^k) killed B10.BR,C3H/HeJ (H-2^k) B10.A (4R) (sharing K^k with B10.BR) and C3H-KBR (sharing D^k with B10.BR) targets, respectively ; however killing activity was not shown on C57BL/10 (H-2^b) and C3H.SW(H-2^b) targets.
In conclusion, LTB4 antagonist improved mouse skin graft survival on rats. This finding may support that neutrophile play a role in xenogeneic immune responses. Pig effectors recognize mouse class-I antigens and show killing activities on mouse targes. It may be expected that deletion of MHC antigens in xenograft might provide elongation of xenograft survival through the suppression of cellular responses.
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