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Impact of vaccine therapy using nuclear histone H1 on allograft survival in experimental organ transplantation.

Abstract：

BACKGROUND:We recently reported that autoreactive antibody (Ab) against nuclear histone H1 had been identified as an immunosuppressive factor in a rat tolerogenic orthotopic liver transplantation (OLT) model. The present study aimed to determine whether the up-regulation of antihistone H1 Ab by histone H1 vaccination leads to tolerance. METHODS:Histone H1-immunized rats were established by intraperitoneal vaccination with histone H1 at every two-weekly interval. By using mixed lymphocyte reaction (MLR) and heterotopic heart transplantation (HHT), the alloreactive T cell response and allograft survival of histone H1-immunized rats were compared with those of control rats. Cytokine and cellular profiles in histone H1-immunized rats were determined by reverse transcriptase polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and flow cytometry. RESULTS:Immunization with histone H1 in Freund's adjuvant induced alloreactive T cell unresponsiveness and prolonged heterotopic heart allograft survival. It also down-regulated the expression of major histocompatibility complex (MHC) class II and CD25 on splenic cells, elevated the T helper cell type 2 (Th2) skewing index (Interleukin (IL)-4/interferon (IFN)-gamma ratio or IL-4/IL-2 ratio) and modified the serum cytokine profiles. CONCLUSIONS:The present results suggest that histone H1 vaccination of transplant recipients, which leads to the production of immunosuppressive factor and the modification of the cytokine/cellular profiles, has great potential as a tolerance therapy for prospective transplantation.

journal_name

Transpl Immunol

journal_title

Transplant immunology

authors

Nakano T,Goto S,Lai CY,Hsu LW,Ono K,Kawamoto S,Lin YC,Kao YH,Chiang KC,Ohmori N,Goto T,Sato S,Tu CH,Jawan B,Cheng YF,Chen CL

doi

10.1016/j.trim.2007.01.003

subject

Has Abstract

pub_date

2007-04-01 00:00:00

pages

147-52

issue

3

eissn

0966-3274

issn

1878-5492

pii

S0966-3274(07)00004-4

journal_volume

17

pub_type

杂志文章

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