Effect of KRN7000 on induced graft-vs-host disease

Morecki, Shoshana; Panigrahi, Soumya; Pizov, Galina; Yacovlev, Elena; Gelfand, Yael; Eizik, Osnat; Slavin, Shimon

doi:10.1016/j.exphem.2004.04.005

Cited by 39 publications

(23 citation statements)

References 42 publications

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“…In this regard, CD4 ϩ CD25 ϩ T cells differ in suppressive activity from the NKT cells, because both donor and host NKT cells have been shown to inhibit GVHD in MHC-mismatched systems (9,11). The suppressive activity of host NKT cells has been reported to be enhanced by activation with the NKT cellspecific ligand, ␣-GalCer (14,28). Enhancement of the GVHD suppressive activity and facilitation of the tumor killing activity of CD8 T cells by donor NKT cells has been reported after treatment of the donors with the fusion protein progenipoietin-1, a potent chimeric cytokine that stimulates both G-CSF and Flt-3L receptors (29).…”

Section: Discussionmentioning

confidence: 99%

Host NKT Cells Can Prevent Graft-versus-Host Disease and Permit Graft Antitumor Activity after Bone Marrow Transplantation

Pillai

George

Dutt

et al. 2007

The Journal of Immunology

128

158

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Allogeneic bone marrow transplantation is a curative treatment for leukemia and lymphoma, but graft-vs-host disease (GVHD) remains a major complication. Using a GVHD protective nonmyeloablative conditioning regimen of total lymphoid irradiation and antithymocyte serum (TLI/ATS) in mice that has been recently adapted to clinical studies, we show that regulatory host NKT cells prevent the expansion and tissue inflammation induced by donor T cells, but allow retention of the killing activity of donor T cells against the BCL1 B cell lymphoma. Whereas wild-type hosts given transplants from wild-type donors were protected against progressive tumor growth and lethal GVHD, NKT cell-deficient CD1d−/− and Jα-18−/− host mice given wild-type transplants cleared the tumor cells but died of GVHD. In contrast, wild-type hosts given transplants from CD8−/− or perforin−/− donors had progressive tumor growth without GVHD. Injection of host-type NKT cells into Jα-18−/− host mice conditioned with TLI/ATS markedly reduced the early expansion and colon injury induced by donor T cells. In conclusion, after TLI/ATS host conditioning and allogeneic bone marrow transplantation, host NKT cells can separate the proinflammatory and tumor cytolytic functions of donor T cells.

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Section: Discussionmentioning

confidence: 99%

Host NKT Cells Can Prevent Graft-versus-Host Disease and Permit Graft Antitumor Activity after Bone Marrow Transplantation

Pillai

George

Dutt

et al. 2007

The Journal of Immunology

128

158

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“…Although most studies suggest that ␣-GalCer prevents autoimmunity by promoting T H 2 responses, it is becoming clear that the induction of tolerogenic DCs 50 or regulatory T cells may also have a crucial role. 51 Administration of ␣-GalCer to recipients in a mouse model of allogeneic SCT after sublethal irradiation significantly reduced GVHD, 52 subsequently shown to be associated with T H 2 polarization of donor T cells. 53 Haraguchi et al, 54 using a nonlethal irradiation BMT model, confirmed that residual host iNKT cells provided protection from GVHD.…”

Section: Effects Of Stem Cell Mobilization With Novel G-csf Analogsmentioning

confidence: 99%

Stem cell mobilization with G-CSF analogs: a rational approach to separate GVHD and GVL?

Morris

MacDonald

Hill

2006

Blood

100

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“…(Morecki et al, 2004) Briefly, F 1 recipients were lethally irradiated (900 cGy total, divided into two doses of 450 cGy given over 24 h). Six hours after irradiation, 10 · 10 6 B6 BM cells and 30 · 10 6 B6 spleen cells were injected in 200 ll of PBS via lateral tail vein injection (GVHD inoculum).…”

Section: Mspc Administrationmentioning

confidence: 99%

Murine bone marrow derived stromal progenitor cells fail to prevent or treat acute graft‐versus‐host disease

Badillo¹,

Peranteau²,

Heaton

et al. 2008

Br J Haematol

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SummaryHuman and murine stromal progenitor cells (SPCs) can suppress alloresponse in vitro, suggesting that SPCs may have clinical application toward prevention or treatment of graft‐versus‐host disease (GVHD). However, th eresults of in vivo studies have been conflicting. This study utilized an established murine model of acute GVHD to assess the ability of bone marrow derived murine SPCs (mSPCs) to prevent or treat GVHD. GVHD was established by transplantation of B6 bone marrow and spleen cells into lethally irradiated (900 cGy) B6 × BALB/c F1 recipients. mSPCs were administered using various dose and timing protocols designed to either prevent or treat GVHD. After transplantation, mice were monitored daily for weight and survival. Differences in symptom severity were compared using a clinical GVHD scoring system. All GVHD control mice died of lethal GVHD. All groups treated with mSPCs for the prevention of GVHD went on to develop clinical GVHD with no alteration of the disease course or severity compared to controls. Administration of mSPC after the development of GVHD failed to improve the disease course. We conclude that in this model, the ability of SPCs to suppress alloresponse in vitro does not correlate with in vivo prevention or treatment of acute GVHD.

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Effect of KRN7000 on induced graft-vs-host disease

Cited by 39 publications

References 42 publications

Host NKT Cells Can Prevent Graft-versus-Host Disease and Permit Graft Antitumor Activity after Bone Marrow Transplantation

Host NKT Cells Can Prevent Graft-versus-Host Disease and Permit Graft Antitumor Activity after Bone Marrow Transplantation

Stem cell mobilization with G-CSF analogs: a rational approach to separate GVHD and GVL?

Murine bone marrow derived stromal progenitor cells fail to prevent or treat acute graft‐versus‐host disease

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