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http://purl.uniprot.org/citations/31634333http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31634333http://www.w3.org/2000/01/rdf-schema#comment"

Background

Gastrointestinal acute graft-versus-host disease (GVHD) occurring after allogeneic hematopoietic cell transplant is an allo-reactive T cell and inflammatory cytokine driven organ injury with epithelial apoptosis as 1 of its hallmark findings and is associated with significant mortality. Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNFAIP8 or TIPE) acts as a negative mediator of apoptosis via inhibition of caspase-3 activation, promotes cell proliferation and Tipe deficiency is associated with increased inflammation.

Methods

To evaluate the role of TIPE in acute GVHD, naive C57BL/6 and Tipe C57BL/6 mice were conditioned with 1000 cGy single dose total body irradiation, followed by transplantation of 10 million bone marrow cells and 20 million splenocytes from either syngeneic C57BL/6 or allogeneic BALB/c donors.

Results

Allo TIPE-deficient mice developed exacerbated gut GVHD compared with allo controls and had significantly decreased survival (6 wk overall survival: 85% versus 37%; P < 0.05), higher clinical GVHD scores, more profound weight loss, increased serum proinflammatory cytokines (interleukin-17A, TNF, interleukin-6, and interferon-γ). T-cell infiltration into the ileum was increased; epithelial proliferation was decreased along with significantly higher levels of chemokines KC and monokine induced by gamma interferon. Using bone marrow chimeric experiments, TIPE was found to have a role in both hematopoietic and nonhematopoietic cells.

Conclusions

Absence of TIPE results in excessive inflammation and tissue injury after allo-HCT, supporting that TIPE confers immune homeostasis and has tissue-protective function during the development of gut GVHD and may be a potential future target to prevent or treat this complication after allogeneic HCT."xsd:string
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http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Du J."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Chen Y.H."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Huang T."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Kumari R."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Kohler K."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Kesler M.V."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Palaniyandi S."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Hildebrandt G.C."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Strattan E."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Dalland J."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/author"Jabbour N."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/name"Transplantation"xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/pages"500-510"xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/title"TNFAIP8 Deficiency Exacerbates Acute Graft Versus Host Disease in a Murine Model of Allogeneic Hematopoietic Cell Transplantation."xsd:string
http://purl.uniprot.org/citations/31634333http://purl.uniprot.org/core/volume"104"xsd:string
http://purl.uniprot.org/citations/31634333http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31634333
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