Cytokines in Graft-versus-Host Disease

Henden, Andrea S.; Hill, Geoffrey R.

doi:10.4049/jimmunol.1500117

Cited by 154 publications

(129 citation statements)

References 133 publications

(108 reference statements)

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“…15,16 In mice with GVHD, early after BMT (day 7), donor NK cells in all tissues expressed increased levels of CD69 relative to donor NK cells in syngeneic BMT recipients ( Figure 2D). By days 14 and 28 posttransplant the overall expression level of CD69 had decreased, but was still For personal use only.…”

Section: Donor Nk Cells Are Activated During Gvhdmentioning

confidence: 99%

GVHD prevents NK-cell–dependent leukemia and virus-specific innate immunity

Bunting

Varelias

Souza-Fonseca-Guimarães

et al. 2017

Blood

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Key Points• Donor T cells compete for IL-15 with NK cells during GVHD, resulting in profound defects in NK-cell reconstitution.• GVHD impairs NK-celldependent leukemia and pathogen-specific immunity.Allogeneic bone marrow transplantation (allo-BMT) is a curative therapy for hematological malignancies, but is associated with significant complications, principally graftversus-host disease (GVHD) and opportunistic infections. Natural killer (NK) cells mediate important innate immunity that provides a temporal bridge until the reconstruction of adaptive immunity. Here, we show that the development of GVHD after allo-BMT prevented NK-cell reconstitution, particularly within the maturing M1 and M2 NK-cell subsets in association with exaggerated activation, apoptosis, and autophagy. Donor T cells were critical in this process by limiting the availability of interleukin 15 (IL-15), and administration of IL-15/IL-15Ra or immune suppression with rapamycin could restore NK-cell reconstitution. Importantly, the NK-cell defect induced by GVHD resulted in the failure of NK-cell-dependent in vivo cytotoxicity and graft-versus-leukemia effects.Control of cytomegalovirus infection after allo-BMT was also impaired during GVHD. Thus, during GVHD, donor T cells compete with NK cells for IL-15 thereby inducing profound defects in NK-cell reconstitution that compromise both leukemia and pathogen-specific immunity. (Blood. 2017;129(5):630-642)

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Section: Donor Nk Cells Are Activated During Gvhdmentioning

confidence: 99%

GVHD prevents NK-cell–dependent leukemia and virus-specific innate immunity

Bunting

Varelias

Souza-Fonseca-Guimarães

et al. 2017

Blood

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“…After allo-HSCT, various inflammatory cytokine levels are significantly increased 25,26 and seem to be associated with complications, such as sinusoidal obstructive syndrome and GVHD. In addition to lymphocyte-secreted cytokines, adipocytederived cytokines may have a role in the development of insulin resistance and subsequent type 2 DM.…”

Section: Inflammationmentioning

confidence: 99%

How do I manage hyperglycemia/post-transplant diabetes mellitus after allogeneic HSCT

Fuji

Rovó

Ohashi

et al. 2016

Bone Marrow Transplant

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Allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipients frequently develop glucose intolerance and post-transplant diabetes mellitus (PTDM). The clinical importance of PTDM and its detrimental impact on HSCT outcomes are underrecognized. After allo-HSCT, various mechanisms can contribute to the development of PTDM. Here we review information about hyperglycemia and PTDM after allo-HSCT as well as PTDM after solid organ transplantation and describe ways to manage hyperglycemia/PTDM after allogeneic HSCT. Taking into consideration a lack of well-established evidence in the field of allo-HSCT, more studies should be conducted in the future, which will require closer multidisciplinary collaboration between hematologists, endocrinologists and nutritionists.

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“…Expression of integrins and their respective ligands plays an important role in homing of donor T cells to Peyer's patches during aGVHD. The GI tract is especially susceptible to damage from TNFα and the GI tract play a major role in generation of the cytokine storm that is the characteristic of aGVHD (4). TNFα can be produced by both donor and host cells and produces myriad of effects including activation of APCs and alloantigen presentation, localization of immune effector cells to the target organs via increased chemokine production and causing direct tissue necrosis.…”

Section: Gvhd Pathophysiologymentioning

confidence: 99%

Graft-versus-host disease management

Mistrík¹,

Bojtárová²,

Sopko³

et al. 2016

BLL

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Graft-versus-host disease (GVHD) remains a major problem of allogeneic hematopoietic-stem cell transplantation (HSCT) and an obstacle for successful outcome. Clinically signifi cant acute GVHD (grade II or higher) developed in 20 to 65 percent of the patients. Death due to this complication accounts for approximately 50 percent of the deaths that are not due to a relapse of the neoplasm. Up to 70 % of patients who survive beyond day 100 develop chronic GVHD and it is the leading cause of nonrelapse mortality more than 2 years after allogeneic HSCT. In addition, chronic GVHD is associated with decreased quality of life, impaired functional status, and ongoing need for immunosuppressive medications. The incidence of chronic GVHD is increasing because of expansion of the donor population beyond HLA-identical siblings, older recipient age, use of peripheral blood cells as the graft source, and infusion of donor lymphocytes for treatment of recurrent malignancy after HSCT. With the current rush in new fi ndings related to GVHD, we see a signifi cant advancement in its management. Given these various new options and challenges, it is important to identify the minimal requirements for diagnosis and treatment of GVHD, as access to the most sophisticated advances may vary depending on local circumstances (Tab. 4, Fig. 1, Ref. 51). Text in PDF www.elis.sk.

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Cytokines in Graft-versus-Host Disease

Cited by 154 publications

References 133 publications

GVHD prevents NK-cell–dependent leukemia and virus-specific innate immunity

GVHD prevents NK-cell–dependent leukemia and virus-specific innate immunity

How do I manage hyperglycemia/post-transplant diabetes mellitus after allogeneic HSCT

Graft-versus-host disease management

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