scholarly journals Combined Th2 cytokine deficiency in donor T cells aggravates experimental acute graft-vs-host disease

2008 ◽  
Vol 36 (8) ◽  
pp. 988-996 ◽  
Author(s):  
Isao Tawara ◽  
Yoshinobu Maeda ◽  
Yaping Sun ◽  
Kathleen P. Lowler ◽  
Chen Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Host Disease ◽  
Th2 Cytokine ◽  
Graft Vs Host Disease ◽  
Donor T Cells ◽  
Acute Graft

scholarly journals Allosuppressor and allohelper T cells in acute and chronic graft-vs-host disease. V. F1 mice with secondary chronic GVHD contain F1-reactive allohelper but no allosuppressor T cells.

1984 ◽  
Vol 159 (2) ◽  
pp. 508-523 ◽  
Author(s):  
S T Pals ◽  
H Gleichmann ◽  
E Gleichmann
Keyword(s):  
T Cells ◽  
Early Stage ◽  
Chronic Gvhd ◽  
Third Party ◽  
Th Cells ◽  
Host Disease ◽  
Graft Vs Host Disease ◽  
Donor T Cells ◽  
Split Tolerance ◽  
B10 Cells

We studied the alloreactive properties of donor T cells obtained from F1 mice that had recovered from the allosuppression of acute graft-vs.-host disease (GVHD) and showed mild symptoms of chronic GVHD, i.e., so-called secondary chronic GVHD. To this end, we used (B10 x DBA/2)F1 mice that had been injected with 10(8) B10 spleen cells 100-150 d previously. Such GVHD F1 mice were repopulated by lympho-hematopoietic cells of donor (B10) origin, which exhibited split tolerance towards the host: Whereas F1-specific donor T helper (Th) cells as well as T cells proliferating in the mixed lymphocyte reaction were readily demonstrable, F1-specific T suppressor (Ts) and T killer (Tk) cells were not, or were hardly, detectable; responses against third-party alloantigens were normal. Upon adoptive transfer to nonirradiated secondary recipients, the B10 cells obtained from the repopulated GVH F1 mice induced F1-specific enlargement of the draining popliteal lymph node and enhancement of the IgG formation therein. B10 cells of the same kind were unable, however, to induce lethal GVHD upon transfer to 950 rad-irradiated secondary (B10 x DBA/2)F1 recipients. We conclude that alloactivated donor Ts/Tk cells disappear from the host at a relatively early stage of GVHD, i.e., at the end of acute GVHD , presumably because they are short-lived. By contrast, the longevity of alloactivated donor Th cells causes the symptoms of secondary chronic GVHD.

scholarly journals Tissue-specific regulatory T cells: biomarker for acute graft-vs-host disease and survival

2012 ◽  
Vol 40 (12) ◽  
pp. 974-982.e1 ◽  
Author(s):  
Brian G. Engelhardt ◽  
Salyka M. Sengsayadeth ◽  
Madan Jagasia ◽  
Bipin N. Savani ◽  
Adetola A. Kassim ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Tissue Specific ◽  
Host Disease ◽  
Graft Vs Host Disease ◽  
Acute Graft

scholarly journals Interleukin-18 Regulates Acute Graft-Versus-Host Disease by Enhancing Fas-mediated Donor T Cell Apoptosis

2001 ◽  
Vol 194 (10) ◽  
pp. 1433-1440 ◽  
Author(s):  
Pavan Reddy ◽  
Takanori Teshima ◽  
Mark Kukuruga ◽  
Rainer Ordemann ◽  
Chen Liu ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Graft Versus Host Disease ◽  
Acute Gvhd ◽  
Host Disease ◽  
Murine Bone Marrow ◽  
Graft Versus Host ◽  
Donor T Cells ◽  
Ifn Γ ◽  
Acute Graft

Interleukin (IL)-18 is a recently discovered cytokine that modulates both T helper type 1 (Th1) and Th2 responses. IL-18 is elevated during acute graft-versus-host disease (GVHD). We investigated the role of IL-18 in this disorder using a well characterized murine bone marrow transplantation (BMT) model (B6 → B6D2F1). Surprisingly, blockade of IL-18 accelerated acute GVHD-related mortality. In contrast, administration of IL-18 reduced serum tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS) levels, decreased intestinal histopathology, and resulted in significantly improved survival (75 vs. 15%, P < 0.001). Administration of IL-18 attenuated early donor T cell expansion and was associated with increased Fas expression and greater apoptosis of donor T cells. The administration of IL-18 no longer protected BMT recipients from GVHD when Fas deficient (lpr) mice were used as donors. IL-18 also lost its ability to protect against acute GVHD when interferon (IFN)-γ knockout mice were used as donors. Together, these results demonstrate that IL-18 regulates acute GVHD by inducing enhanced Fas-mediated apoptosis of donor T cells early after BMT, and donor IFN-γ is critical for this protective effect.

scholarly journals MiR-223 Derived from Mesenchymal Stem Cell Exosomes Alleviates Acute Graft-Versus-Host Disease

2020 ◽  
Author(s):  
Weijiang Liu ◽  
Na Zhou ◽  
Peng Wang ◽  
Yuanlin Liu ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Mesenchymal Stem Cells ◽  
Graft Versus Host Disease ◽  
High Throughput Sequencing ◽  
Human Umbilical Cord ◽  
Host Disease ◽  
Graft Versus Host ◽  
Donor T Cells ◽  
Acute Graft

Abstract Background Mesenchymal stem cells (MSCs) have been utilized in treating acute graft-versus-host disease (aGvHD) as they show strong immunosuppressive capacity, but the mechanisms are not well defined.Methods In this study, we demonstrated that microRNA-223 (miR-223) derived from exosomes secreted by human umbilical cord mesenchymal stem cells (huc-MSCs) and murine compact bone mesenchymal stem cells (mb-MSCs) could inhibit aGvHD progression by reducing the migration and homing of donor T cells in aGvHD mice.Results MiR-223 was one of the conserved microRNAs highly expressed in huc-MSCs exosomes and mMSCs exosomes, which was identified by high-throughput sequencing. MiR-223 derived from MSC exosomes showed enhanced immunosuppressive capacity, as it could inhibit expression of the target gene ICAM-1 and restrain adhesion and migration of T cells in vitro. Moreover, miR-223Agomir was effective in reducing the inflammatory reaction, and declining the donor T cells infiltration into the spleen, liver and intestine in aGvHD mice. Subsequently, it could alleviate aGvHD symptoms. Taken together, the MSC exosome derived miR-223 could attenuate aGvHD in mice through regulating ICAM-1 expression.Conclusions Our results unveil a new role for MSC exosomes derived miR-223 in the treatment of aGvHD.

Hla-b44.2 directed cytotoxic t cells associated with acute graft vs host disease following unrelated marrow transplantation

1991 ◽  
Vol 32 ◽  
pp. 76
Author(s):  
C.A. Keever ◽  
N. Leong ◽  
I. Cunningham ◽  
E.A. Copelan ◽  
B.R. Avalos ◽  
...  
Keyword(s):  
T Cells ◽  
Marrow Transplantation ◽  
Cytotoxic T Cells ◽  
Host Disease ◽  
Graft Vs Host Disease ◽  
Acute Graft

Lymphopenia-induced proliferation of donor T cells reduces their capacity for causing acute graft-versus-host disease

2007 ◽  
Vol 35 (2) ◽  
pp. 274-286 ◽  
Author(s):  
Yoshinobu Maeda ◽  
Isao Tawara ◽  
Takanori Teshima ◽  
Chen Liu ◽  
Daigo Hashimoto ◽  
...  
Keyword(s):  
T Cells ◽  
Graft Versus Host Disease ◽  
Host Disease ◽  
Graft Versus Host ◽  
Donor T Cells ◽  
Acute Graft
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