scholarly journals Differential Effects of Gut-Homing Molecules CC Chemokine Receptor 9 and Integrin-β7 during Acute Graft-versus-Host Disease of the Liver

2015 ◽  
Vol 21 (12) ◽  
pp. 2069-2078 ◽  
Author(s):  
Alina Schreder ◽  
Georgios Leandros Moschovakis ◽  
Stephan Halle ◽  
Jerome Schlue ◽  
Chun-Wei Lee ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Chemokine Receptor ◽  
Host Disease ◽  
Differential Effects ◽  
Graft Versus Host ◽  
Cc Chemokine ◽  
Acute Graft

scholarly journals R707, a fully human antibody directed against CC-chemokine receptor 7, attenuates xenogeneic acute graft-versus-host disease

2019 ◽  
Vol 19 (7) ◽  
pp. 1941-1954 ◽  
Author(s):  
Kenneth A. Fowler ◽  
Viktoria Vasilieva ◽  
Ekaterina Ivanova ◽  
Olga Rimkevich ◽  
Andrey Sokolov ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Chemokine Receptor ◽  
Human Antibody ◽  
Host Disease ◽  
Graft Versus Host ◽  
Cc Chemokine ◽  
Cc Chemokine Receptor 7 ◽  
Acute Graft

scholarly journals CC chemokine receptor 8 potentiates donor Treg survival and is critical for the prevention of murine graft-versus-host disease

Blood ◽  
2013 ◽  
Vol 122 (5) ◽  
pp. 825-836 ◽  
Author(s):  
James M. Coghill ◽  
Kenneth A. Fowler ◽  
Michelle L. West ◽  
LeShara M. Fulton ◽  
Hendrik van Deventer ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Chemokine Receptor ◽  
Host Disease ◽  
Graft Versus Host ◽  
Cc Chemokine ◽  
Key Points

Key Points Extended donor Treg survival is required for protection from GVHD; donor Treg longevity depends on Treg CCR8 expression. Donor CD11c+ APCs promote Treg longevity in vivo; host CD11c+ APCs do not appear to contribute to donor Treg reconstitution.

scholarly journals Separation of graft-versus-host disease from graft-versus-leukemia responses by targeting CC-chemokine receptor 7 on donor T cells

Blood ◽  
2010 ◽  
Vol 115 (23) ◽  
pp. 4914-4922 ◽  
Author(s):  
James M. Coghill ◽  
Michael J. Carlson ◽  
Angela Panoskaltsis-Mortari ◽  
Michelle L. West ◽  
Joseph E. Burgents ◽  
...  
Keyword(s):  
T Cells ◽  
Graft Versus Host Disease ◽  
Chemokine Receptor ◽  
Critical Role ◽  
Host Disease ◽  
Graft Versus Host ◽  
Cc Chemokine ◽  
Graft Versus Leukemia ◽  
Cc Chemokine Receptor 7

Abstract CC-chemokine receptor 7 (CCR7) is expressed on the surface of naive T cells, and plays a critical role in their movement into secondary lymphoid tissue. Here, we show that murine T cells lacking CCR7 (CCR7−/−) generate attenuated graft-versus-host disease (GVHD) responses compared with wild-type (WT) cells, with the difference varying inversely with the degree of major histocompatibility complex (MHC) disparity between the donor and recipient. CCR7−/− T cells exhibited an impaired ability to traffic to recipient lymph nodes, with an increased capacity to home to the spleen. CCR7−/− T cells, however, demonstrated a reduced ability to undergo in vivo expansion in the spleen due to impaired interactions with splenic antigen-presenting cells. On a cellular level, CCR7−/− T cells were functionally competent, demonstrating a normal in vitro proliferative capacity and a preserved ability to produce inflammatory cytokines. Importantly, CCR7−/− T cells were capable of generating robust graft-versus-leukemia (GVL) responses in vivo, as well as complete donor T-cell reconstitution. CCR7−/− regulatory T cells were able to protect against lethal GVHD when administered before WT conventional T cells. Our data suggest that CCR7 inhibition in the early posttransplantation period may represent a feasible new therapeutic approach for acute GVHD attenuation without compromising GVL responses.

scholarly journals CC Chemokine Receptor 2 Expression in Donor Cells Serves an Essential Role in Graft-versus-Host-Disease

2003 ◽  
Vol 171 (9) ◽  
pp. 4875-4885 ◽  
Author(s):  
Arun R. Rao ◽  
Marlon P. Quinones ◽  
Edgar Garavito ◽  
Yogeshwar Kalkonde ◽  
Fabio Jimenez ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Chemokine Receptor ◽  
Essential Role ◽  
Host Disease ◽  
Graft Versus Host ◽  
Cc Chemokine ◽  
Donor Cells ◽  
Cc Chemokine Receptor 2

scholarly journals Differential effects of proteasome inhibition by bortezomib on murine acute graft-versus-host disease (GVHD): delayed administration of bortezomib results in increased GVHD-dependent gastrointestinal toxicity

Blood ◽  
2005 ◽  
Vol 106 (9) ◽  
pp. 3293-3299 ◽  
Author(s):  
Kai Sun ◽  
Danice E. C. Wilkins ◽  
Miriam R. Anver ◽  
Thomas J. Sayers ◽  
Angela Panoskaltsis-Mortari ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Graft Versus Host Disease ◽  
Proteasome Inhibition ◽  
Allogeneic Bone ◽  
Host Disease ◽  
Differential Effects ◽  
Graft Versus Host ◽  
Gastrointestinal Lesions ◽  
Tnf Α ◽  
Acute Graft

AbstractWe have recently demonstrated that the proteasome inhibitor, bortezomib, administered immediately following murine allogeneic bone marrow transplantation (BMT) resulted in marked inhibition of acute graft-versus-host disease (GVHD) with retention of graft-versus-tumor effects. We now assessed the effects of delayed bortezomib administration (5 or more days after BMT) on GVHD. Recipient C57BL/6 (H2b) mice were lethally irradiated and given transplants of bone marrow cells and splenocytes from major histocompatibility complex (MHC)–disparate BALB/c (H2d) donors. In marked contrast to the effects of bortezomib on GVHD prevention when administered immediately after BMT, delayed bortezomib administration resulted in significant acceleration of GVHD-dependent morbidity. No toxicity was observed following delayed bortezomib administration in models where donor T cells were not coadministered, indicating that these deleterious effects were critically dependent on GVHD induction. The increase in GVHD susceptibility even occurred when late administration of bortezomib was preceded by early administration. Pathologic assessment revealed that significant increases in gastrointestinal lesions occurred following delayed bortezomib administration during GVHD. This pathology correlated with significant increases of type 1 tumor necrosis factor α (TNF-α) receptor transcription in gastrointestinal cells and with significant increases of TNF-α, interleukin 1β (IL-1β), and IL-6 levels in the serum. These results indicate that the differential effects of proteasome inhibition with bortezomib on GVHD are critically dependent on the timing of bortezomib administration.

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