CD4+ Invariant Natural Killer T Cells Protect from Acute Graft-Versus-Host Disease Lethality through a Dramatic Expansion of Donor-Derived CD4+FoxP3+ Regulatory T Cells

Schneidawind, Dominik; Pierini, Antonio; Pan, Yuqiong; Baker, Jeanette; Kim, Byung Su; Nishikii, Hidekazu; Büchele, Corina; Meyer, Everett; Negrin, Robert S.

doi:10.1016/j.bbmt.2013.12.004

Cited by 2 publications

(1 citation statement)

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“…Low numbers of iNKT in the donor inoculum have been inversely correlated with clinical GVHD (Chaidos et al , ). Experiments in mice have shown infusion of donor iNKT cells, expanded in vitro , attenuates experimental GVHD by increasing Tregs (Schneidawind et al , ). Despite infusion of cell numbers that are rejected following HCT, evidence suggests that third party iNKTs are similarly capable of suppressing GVHD through induction of natural Tregs while preserving GVL responses.…”

Section: Cellular Mediators Of Peripheral Tolerancementioning

confidence: 99%

Advances in understanding the pathogenesis of graft‐versus‐host disease

2016

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Allogeneic haematopoietic stem cell transplantation (HCT) is a potent immunotherapy with curative potential for several haematological disorders. Overcoming the immunological barrier of acute graft-versus-host disease (GVHD) remains a fundamental impediment to expanding the efficacy of HCT. GVHD reflects a complex pathological interaction between the innate and adaptive immune systems of the host and donor. Over the past decade there has been a tremendous advancement in our understanding of the cellular and molecular underpinnings of this devastating disease. In this review, we cover several recently appreciated facets of GVHD pathogenesis including novel extracellular mediators of inflammation, immune subsets, intracellular signal transduction, post-translation modifications and epigenetic regulation. We begin to develop general themes regarding the immunological pathways in GVHD pathogenesis, discuss critical outstanding questions, and explore new avenues for GVHD treatment and prevention.

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Section: Cellular Mediators Of Peripheral Tolerancementioning

confidence: 99%

Advances in understanding the pathogenesis of graft‐versus‐host disease

2016

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Next generation treatment of acute graft-versus-host disease

Magenau

Reddy

2014

Leukemia

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Despite rapid increase in the utilization of allogeneic hematopoietic stem cell transplantation, non-relapse mortality and sequela from acute graft-versus-host disease (GVHD) remain principle barriers. GVHD involves complex interactions between innate and adaptive immunity, culminating in tissue damage by inflammatory mediators and cellular effectors. Recently, our understanding of the molecular intricacies of GVHD has grown tremendously. New insights into the roles played by novel cytokines, chemokines, intracellular signaling pathways, epigenetics and post-translational modifications of proteins in GVHD biology provide numerous targets that might be therapeutically exploited. This review highlights recent advances and identifies opportunities for reshaping contemporary GVHD therapeutics.

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CD4+ Invariant Natural Killer T Cells Protect from Acute Graft-Versus-Host Disease Lethality through a Dramatic Expansion of Donor-Derived CD4+FoxP3+ Regulatory T Cells

Cited by 2 publications

References 0 publications

Advances in understanding the pathogenesis of graft‐versus‐host disease

Advances in understanding the pathogenesis of graft‐versus‐host disease

Next generation treatment of acute graft-versus-host disease

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