Induction of indirect donor-specific hyporesponsiveness by transportal RT1-peptide pulse in rat skin transplantation

Masao Yamamura, Takahito Yagi, Hiromi Iwagaki, Naoshi Mitsuoka, Liu Jie, Sun Dong Sheng, Hiroaki Matsuda, Hiroshi Sadamori, Masaru Inagaki, Noriaki Tanaka

Research output: Contribution to journalArticle

Abstract

In the present study, we examined whether transportal pulse of class I major histocompatibility complex (MHC) allopeptides can induce indirect (non-chimeric) donor-specific hyporesponsiveness, using a high-responder rat skin transplantation model. Two donor-specific 8-amino acid peptides corresponding to residues 58-65 and 70-77 in the α1 helical region of RT1.Aa were synthesized. In order to test immunogenicity of these peptides, mixed lymphocyte reaction (MLR) was performed. Then, 100-μg portions of peptides were injected into recipient Lewis (LEW, RT1.A1) rats via the portal vein 14 days before skin transplantation. Skin allografts from August Copenhagen Irish (ACI, RT1a) or Wistar King A (WKA, RT1k, third-party) donors were transplanted to LEW (RT11) recipients. Transportal pulse of residues 58-65 and 70-77 prolonged graft survival significantly in ACI-to-LEW skin transplantation (17.6 ± 0.40 and 18.0 ± 0.45 days) compared with control (14.2 ± 0.37 days). However, pulse of residues 106-113, a non-donor-specific control, did not prolong graft survival time (14.6 ± 0.40 days) in the same combination. Regarding the third-party donor, residues 58-65 injected into LEW recipients had no effect on survival time of skin grafts (19.0 ± 0.84 days) derived from WKA donors compared with the untreated WKA-to-LEW control (19.4 ± 0.93 days). Transportal pulse of RT1.Aa peptides induced donors-pecific hyporesponsiveness even in a high-responder rat skin transplantation model. Our results suggest that graft enhancement by transportal exposure to donor cells may not be induced by a chimeric process but, instead, by an indirect mechanism not involving intervention of viable donor cells.

Original languageEnglish
Pages (from-to)549-553
Number of pages5
JournalTransplant international : official journal of the European Society for Organ Transplantation
Volume16
Issue number8
DOIs
Publication statusPublished - Aug 1 2003

Fingerprint

Skin Transplantation
Pulse
Peptides
Graft Survival
Immunologic Graft Enhancement
Skin
Mixed Lymphocyte Culture Test
Portal Vein
Major Histocompatibility Complex
Allografts
Transplants
Amino Acids

Keywords

  • Class I major histocompatibility complex
  • Immunohyporesponsiveness
  • RT1.A
  • Skin transplantation

ASJC Scopus subject areas

  • Transplantation

Cite this

Induction of indirect donor-specific hyporesponsiveness by transportal RT1-peptide pulse in rat skin transplantation. / Yamamura, Masao; Yagi, Takahito; Iwagaki, Hiromi; Mitsuoka, Naoshi; Jie, Liu; Sheng, Sun Dong; Matsuda, Hiroaki; Sadamori, Hiroshi; Inagaki, Masaru; Tanaka, Noriaki.

In: Transplant international : official journal of the European Society for Organ Transplantation, Vol. 16, No. 8, 01.08.2003, p. 549-553.

Research output: Contribution to journalArticle

Yamamura, Masao ; Yagi, Takahito ; Iwagaki, Hiromi ; Mitsuoka, Naoshi ; Jie, Liu ; Sheng, Sun Dong ; Matsuda, Hiroaki ; Sadamori, Hiroshi ; Inagaki, Masaru ; Tanaka, Noriaki. / Induction of indirect donor-specific hyporesponsiveness by transportal RT1-peptide pulse in rat skin transplantation. In: Transplant international : official journal of the European Society for Organ Transplantation. 2003 ; Vol. 16, No. 8. pp. 549-553.
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abstract = "In the present study, we examined whether transportal pulse of class I major histocompatibility complex (MHC) allopeptides can induce indirect (non-chimeric) donor-specific hyporesponsiveness, using a high-responder rat skin transplantation model. Two donor-specific 8-amino acid peptides corresponding to residues 58-65 and 70-77 in the α1 helical region of RT1.Aa were synthesized. In order to test immunogenicity of these peptides, mixed lymphocyte reaction (MLR) was performed. Then, 100-μg portions of peptides were injected into recipient Lewis (LEW, RT1.A1) rats via the portal vein 14 days before skin transplantation. Skin allografts from August Copenhagen Irish (ACI, RT1a) or Wistar King A (WKA, RT1k, third-party) donors were transplanted to LEW (RT11) recipients. Transportal pulse of residues 58-65 and 70-77 prolonged graft survival significantly in ACI-to-LEW skin transplantation (17.6 ± 0.40 and 18.0 ± 0.45 days) compared with control (14.2 ± 0.37 days). However, pulse of residues 106-113, a non-donor-specific control, did not prolong graft survival time (14.6 ± 0.40 days) in the same combination. Regarding the third-party donor, residues 58-65 injected into LEW recipients had no effect on survival time of skin grafts (19.0 ± 0.84 days) derived from WKA donors compared with the untreated WKA-to-LEW control (19.4 ± 0.93 days). Transportal pulse of RT1.Aa peptides induced donors-pecific hyporesponsiveness even in a high-responder rat skin transplantation model. Our results suggest that graft enhancement by transportal exposure to donor cells may not be induced by a chimeric process but, instead, by an indirect mechanism not involving intervention of viable donor cells.",
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AU - Yagi, Takahito

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AU - Mitsuoka, Naoshi

AU - Jie, Liu

AU - Sheng, Sun Dong

AU - Matsuda, Hiroaki

AU - Sadamori, Hiroshi

AU - Inagaki, Masaru

AU - Tanaka, Noriaki

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