XIAP deficiency in hematopoietic recipient cells drives donor T‐cell activation and GvHD in mice

Patients with X‐linked lymphoproliferative syndrome type 2 (XLP‐2) (BIRC4 deficiency) suffer from hyperinflammation often observed during the conditioning regimen prior to allogeneic bone marrow transplant. This article shows that in mice hematopoietic recipient cells contribute to graft‐versus‐host...

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Bibliographic Details
Published in:European journal of immunology 2019-03, Vol.49 (3), p.504-507
Main Authors: Müller, Nicole, Fischer, Julius C., Yabal, Monica, Haas, Tobias, Poeck, Hendrik, Jost, Philipp J.
Format: Article
Language:English
Subjects:
allogeneic HSC transplantation
Animals
Bone marrow
Bone marrow transplantation
Bone Marrow Transplantation - methods
Cell activation
Cytokines
Cytokines - metabolism
Genetic Diseases, X-Linked - genetics
Genetic Diseases, X-Linked - metabolism
Genetic Diseases, X-Linked - therapy
Graft Survival
Graft vs Host Disease - genetics
Graft vs Host Disease - metabolism
Graft-versus-host reaction
Graft‐versus‐host disease
Hematopoietic Stem Cell Transplantation - methods
Humans
IL‐1β
Inflammation
Inflammation Mediators - metabolism
Inhibitor of Apoptosis Proteins - deficiency
Inhibitor of Apoptosis Proteins - genetics
Lymphocyte Activation
Lymphocytes
Lymphoproliferative Disorders - genetics
Lymphoproliferative Disorders - metabolism
Lymphoproliferative Disorders - therapy
Mice
Mice, Inbred C57BL
Mice, Knockout
mixed lymphocytes reaction
T-Lymphocytes - metabolism
Tissue Donors
Transplantation, Homologous
XIAP protein
X‐linked lymphoproliferative syndrome
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Description
Summary:Patients with X‐linked lymphoproliferative syndrome type 2 (XLP‐2) (BIRC4 deficiency) suffer from hyperinflammation often observed during the conditioning regimen prior to allogeneic bone marrow transplant. This article shows that in mice hematopoietic recipient cells contribute to graft‐versus‐host disease by the secretion of elevated levels of proinflammatory cytokines during engraftment when BIRC4 is absent.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.201847818