| Literature DB >> 28057639 |
Ryan H Moy1,2, Austin P Huffman1,3,4, Lee P Richman1, Lisa Crisalli1, Ximi K Wang3,4, James A Hoxie1, Rosemarie Mick1,5, Stephen G Emerson6, Yi Zhang7, Robert H Vonderheide1, David L Porter1, Ran Reshef1,3,4,6.
Abstract
Graft-versus-host disease (GVHD) is a major cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Lymphocyte trafficking via chemokine receptors such as CCR5 plays a critical role in alloreactive responses, and previous data suggest that CCR5 blockade with maraviroc results in a low incidence of visceral GVHD. However, the full scope of clinical and immunologic effects of CCR5 blockade in HSCT has not been described. We compared a cohort of patients enrolled on a trial of reduced-intensity allo-HSCT with standard GVHD prophylaxis plus maraviroc to a contemporary control cohort receiving standard GVHD prophylaxis alone. Maraviroc treatment was associated with a lower incidence of acute GVHD without increased risk of disease relapse, as well as reduced levels of gut-specific markers. At day 30, maraviroc treatment increased CCR5 expression on T cells and dampened T-cell activation in peripheral blood without impairing early immune reconstitution or increasing risk for infections. Patients who developed acute GVHD despite maraviroc prophylaxis showed increased T-cell activation, naive T-cell skewing, and elevated serum CXCL9 and CXCL10 levels. Collectively, these data suggest that maraviroc effectively protects against GVHD by modulating alloreactive donor T-cell responses, and that CXCR3 signaling may be an important resistance mechanism to CCR5 blockade in GVHD.Entities:
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Year: 2017 PMID: 28057639 PMCID: PMC5314813 DOI: 10.1182/blood-2016-08-735076
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113