scholarly journals Th2 Cell Therapy of Established Acute Graft-Versus-Host Disease Requires IL-4 and IL-10 and Is Abrogated by IL-2 or Host-Type Antigen-Presenting Cells

2008 ◽  
Vol 14 (9) ◽  
pp. 959-972 ◽  
Author(s):  
Jason E. Foley ◽  
Jacopo Mariotti ◽  
Kaitlyn Ryan ◽  
Michael Eckhaus ◽  
Daniel H. Fowler
Keyword(s):  
Cell Therapy ◽  
Graft Versus Host Disease ◽  
Antigen Presenting Cells ◽  
Host Disease ◽  
Graft Versus Host ◽  
Type Antigen ◽  
Th2 Cell ◽  
Host Type ◽  
Antigen Presenting ◽  
Acute Graft

Recipient nonhematopoietic antigen-presenting cells are sufficient to induce lethal acute graft-versus-host disease

2011 ◽  
Vol 18 (1) ◽  
pp. 135-142 ◽  
Author(s):  
Motoko Koyama ◽  
Rachel D Kuns ◽  
Stuart D Olver ◽  
Neil C Raffelt ◽  
Yana A Wilson ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Antigen Presenting Cells ◽  
Host Disease ◽  
Graft Versus Host ◽  
Antigen Presenting ◽  
Acute Graft

scholarly journals Enhanced allostimulatory activity of host antigen-presenting cells in old mice intensifies acute graft-versus-host disease

2002 ◽  
Vol 109 (9) ◽  
pp. 1249-1256 ◽  
Author(s):  
Rainer Ordemann ◽  
Raymond Hutchinson ◽  
Jeffrey Friedman ◽  
Steven J. Burakoff ◽  
Pavan Reddy ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Antigen Presenting Cells ◽  
Host Disease ◽  
Graft Versus Host ◽  
Antigen Presenting ◽  
Old Mice ◽  
Acute Graft

Distinct roles for donor- and host-derived antigen-presenting cells and costimulatory molecules in murine chronic graft-versus-host disease: requirements depend on target organ

Blood ◽  
2005 ◽  
Vol 105 (5) ◽  
pp. 2227-2234 ◽  
Author(s):  
Britt E. Anderson ◽  
Jennifer M. McNiff ◽  
Dhanpat Jain ◽  
Bruce R. Blazar ◽  
Warren D. Shlomchik ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Cd8 T Cells ◽  
Acute Gvhd ◽  
Dominant Role ◽  
Chronic Gvhd ◽  
Antigen Presenting Cells ◽  
Target Tissue ◽  
Host Disease ◽  
Graft Versus Host ◽  
Antigen Presenting

AbstractThe application of allogeneic stem cell transplantation (alloSCT) is limited by graft-versus-host disease (GVHD). GVHD can be divided into acute and chronic forms that likely have different requirements for initiation and pathogenesis mechanisms. In prior studies we demonstrated that residual host antigen-presenting cells (APCs) were required to initiate acute GVHD (aGVHD) mediated by CD8 T cells. In contrast, here we demonstrate that either donor or host APCs can initiate CD4-mediated GVHD in a model that has features of chronic GVHD (cGVHD). Both donor and host APCs must provide CD80/86-dependent costimulation to elicit maximal cGVHD, and there is no GVHD when both donor and host lack CD80/86. Finally, we were surprised to find that, although either donor or host APCs are sufficient to stimulate skin cGVHD, donor APCs play a dominant role in intestinal cGVHD. Both CD40 and CD80/86 are critical for donor APC function in intestinal cGVHD, but only CD80/86 is required for skin cGVHD. Thus, there are target-tissue–specific differences in APC requirements. These results identify differences in APC requirements between CD8-mediated aGVHD and CD4-mediated cGVHD. They further highlight donor APCs as additional targets for GVHD therapy.

scholarly journals Gas6 deficiency in recipient mice of allogeneic transplantation alleviates hepatic graft-versus-host disease

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3390-3397 ◽  
Author(s):  
Laurent Burnier ◽  
François Saller ◽  
Linda Kadi ◽  
Anne C. Brisset ◽  
Rocco Sugamele ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
T Cell ◽  
Graft Versus Host Disease ◽  
Antigen Presenting Cells ◽  
Allogeneic Bone ◽  
Hematopoietic Stem ◽  
Host Disease ◽  
Graft Versus Host ◽  
Antigen Presenting

Abstract Growth arrest-specific gene 6 (Gas6) is expressed in antigen-presenting cells and endothelial cells (ECs) but not in T cells. When wild-type (WT) or Gas6−/− mice received allogeneic non–T cell–depleted bone marrow cells, hepatic graft-versus-host disease (GVHD) was alleviated in Gas6−/− recipients regardless of donor genotype, but not in WT recipients. T-cell infiltration was more prominent and diffuse in WT than in Gas6−/− recipients' liver. When mice received 0.5 × 106 allogeneic T cells with T cell–depleted allogeneic bone marrow, clinical signs indicated that GVHD was less severe in Gas6−/− than in WT recipients, as shown by a significant improvement of the survival and reduced liver GVHD. These data demonstrate that donor cells were not involved in the protection mechanism. In addition, lack of Gas6 in antigen-presenting cells did not affect WT or Gas6−/− T-cell proliferation. We therefore assessed the response of WT or Gas6−/− ECs to tumor necrosis factor-α. Lymphocyte transmigration was less extensive through Gas6−/− than WT ECs and was not accompanied by increases in adhesion molecule levels. Thus, the lack of Gas6 in ECs impaired donor T-cell transmigration into the liver, providing a rationale for considering Gas6 pathway as a potential nonimmunosuppressive target to minimize GVHD in patients receiving allogeneic hematopoietic stem cell transplantation.

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