HLA-G dimer targets Granzyme B pathway to prolong human renal allograft survival.
Adult
Animals
Antigens, CD
/ metabolism
CD8-Positive T-Lymphocytes
/ metabolism
Concanavalin A
/ pharmacology
Female
Flow Cytometry
Graft Rejection
Graft Survival
Granzymes
/ metabolism
HLA-G Antigens
/ metabolism
Humans
Kidney Transplantation
Leukocyte Immunoglobulin-like Receptor B1
/ antagonists & inhibitors
Mice
Real-Time Polymerase Chain Reaction
T-Lymphocytes
/ metabolism
HLA-G
human kidney transplantation
humanized mouse
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
pubmed:
9
1
2019
medline:
14
1
2020
entrez:
9
1
2019
Statut:
ppublish
Résumé
Human leukocyte antigen G (HLA-G), a nonclassic HLA class Ib molecule involved in the maintenance of maternal tolerance to semiallogeneic fetal tissues during pregnancy, has emerged as a potential therapeutic target to control allograft rejection. We demonstrate here that the level of soluble HLA-G dimer was higher in a group of 90 patients with a functioning renal allograft compared with 40 patients who rejected (RJ) their transplants. The HLA-G dimer level was not affected by demographic status. One of the potential mechanisms in tissue-organ allograft rejection involves the induction of granzymes and perforin, which are the main effector molecules expressed by CD8
Identifiants
pubmed: 30620626
doi: 10.1096/fj.201802017R
pmc: PMC6436663
doi:
Substances chimiques
Antigens, CD
0
HLA-G Antigens
0
LILRB1 protein, human
0
Leukocyte Immunoglobulin-like Receptor B1
0
Concanavalin A
11028-71-0
Granzymes
EC 3.4.21.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
5220-5236Subventions
Organisme : NCI NIH HHS
ID : R01 CA172230
Pays : United States
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