Spontaneous Allograft Tolerance in B7-Deficient Mice Independent of Preexisting Endogenous CD4+CD25+ Regulatory T-Cells

Grazia, Todd J.; Plenter, Robert J.; Doan, An N.; Kelly, Brian P.; Weber, Sarah M.; Kurche, Jonathan S.; Cushing, Susan; Gill, Ronald G.; Pietra, Biagio A.

doi:10.1097/01.tp.0000265482.88936.b1

Cited by 3 publications

(3 citation statements)

References 39 publications

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“…Thus, B7-2 plays a critical role in T-cell activation and proliferation. B7-2 is strongly expressed on endothelial cells and infiltrating mononuclear cells of the cardiac allograft within 24 h post-transplant [13], and blockade of the B7/CD28 co-stimulation pathway has been shown to prolong cardiac allograft survival in numerous rodent models [14,15]. In a lung transplant mice model [16], P. aeruginosa airway infection induced sharply up-regulation of B7 molecules of CD80 and CD86.…”

Section: Discussionmentioning

confidence: 99%

Circulating cytokine portraits can differentiate between allograft rejection and pulmonary infection in cardiac transplant rats

Chen

Zhan

et al. 2016

Interact CardioVasc Thorac Surg

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Section: Discussionmentioning

confidence: 99%

Circulating cytokine portraits can differentiate between allograft rejection and pulmonary infection in cardiac transplant rats

Chen

Zhan

et al. 2016

Interact CardioVasc Thorac Surg

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“…Naïve or “tolerant” leukocytes : Spleens were harvested from naïve B6 mice or long term surviving recipients of αLFA-1 mAb treated allografts according to previously published methods [13]. On POD3–7 heart-grafted recipients were injected with 3×10 7 unfractionated splenocytes i.p.…”

Section: Methodsmentioning

confidence: 99%

Anti-LFA-1 induces CD8 T-cell dependent allograft tolerance and augments suppressor phenotype CD8 cells

Plenter

Grazia

Coulombe

et al. 2018

Cellular Immunology

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The induction of tolerance to transplanted organs is a major objective in transplantation immunology research. Lymphocyte function-associated antigen-1 (LFA-1) interactions have been identified as a key component of the T-cell activation process that may be interrupted to lead to allograft tolerance. In mice, αLFA-1 mAb is a potent monotherapy that leads to the induction of donor-specific transferable tolerance. By interrogating important adaptive and innate immunity pathways, we demonstrate that the induction of tolerance relies on CD8T-cells. We further demonstrate that αLFA-1 induced tolerance is associated with CD8CD28T-cells with a suppressor phenotype, and that while CD8 cells are present, the effector T-cell response is abrogated. A recent publication has shown that CD8CD28 cells are not diminished by cyclosporine or rapamycin, therefore CD8CD28 cells represent a clinically relevant population. To our knowledge, this is the first time that a mechanism for αLFA-1 induced tolerance has been described.

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“…Mixed lymphocyte reactions (MLR) with recipient‐type B6 lymph node responder cells and BALB/c or C3H stimulator splenocytes were performed as previously published (39, 40). B6 CD117 + PC, B6 CD117 − effluent cells, or B6 bone marrow cells were added (at BM rations of 1:1–1:256 with responders).…”

Section: Methodsmentioning

confidence: 99%

Prolongation of Cardiac Allograft Survival by a Novel Population of Autologous CD117+ Bone Marrow-Derived Progenitor Cells

Grazia

Plenter

Lepper

et al. 2011

American Journal of Transplantation

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Autologous CD117+ progenitor cells (PC) have been successfully utilized in myocardial infarction and ischemic injury, potentially through the replacement/repair of damaged vascular endothelium. To date, such cells have not been used to enhance solid organ transplant outcome. In this study, we determined whether autologous bone marrow-derived CD117 + PC could benefit cardiac allograft survival, possibly by replacing donor vascular cells. Autologous, positively selected CD117 + PC were administered posttransplantation and allografts were assessed for acute rejection. Although significant generation of recipient vascular cell chimerism was not observed, transferred PC disseminated both to the allograft and to peripheral lymphoid tissues and facilitated a significant, dosedependent prolongation of allograft survival. While CD117 + PC dramatically inhibited alloreactive T cell proliferation in vitro, this property did not differ from nonprotective CD117 − bone marrow populations. In vivo, CD117+ PC did not significantly inhibit T cell alloreactivity or increase peripheral regulatory T cell numbers. Thus, rather than inhibiting adaptive immunity to the allograft, CD117+ PC may play a cytoprotective role in prolonging graft survival. Importantly, autologous CD117+ PC appear to be distinct from bone marrow-derived mesenchymal stem cells (MSC) previously used to prolong allograft survival. As such, autologous CD117 + PC represent a novel cellular therapy for promoting allograft survival.

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Spontaneous Allograft Tolerance in B7-Deficient Mice Independent of Preexisting Endogenous CD4+CD25+ Regulatory T-Cells

Cited by 3 publications

References 39 publications

Circulating cytokine portraits can differentiate between allograft rejection and pulmonary infection in cardiac transplant rats

Circulating cytokine portraits can differentiate between allograft rejection and pulmonary infection in cardiac transplant rats

Anti-LFA-1 induces CD8 T-cell dependent allograft tolerance and augments suppressor phenotype CD8 cells

Prolongation of Cardiac Allograft Survival by a Novel Population of Autologous CD117+ Bone Marrow-Derived Progenitor Cells

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