Linked Life Data

20197103

Source:http://linkedlifedata.com/resource/pubmed/id/20197103

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-5-10
pubmed:abstractText
Donor NK cells have been shown to be able to promote engraftment during allogeneic bone marrow transplantation. They could specifically suppress or delete host reactive cells, thereby facilitating engraftment of donor marrow. To further elucidate the mechanism, we showed that activated H2(d) ALAK cells (adherent lymphokine activated killer, IL-2 activated T cell-depleted bone marrow and spleen cells) from BALB/c mice significantly suppressed the proliferation of H2(b) splenocytes from C57BL/6 mice in mixed lymphocyte responses (MLR) stimulated with irradiated H2(d) splenocytes from BALB/c mice (P < .01). The ability for H2(b) splenocytes to kill H2(d) tumor targets was also significantly inhibited by activated H2(d) ALAK cells (P < .01). The same number of H2(b) ALAK cells or H2(d) splenocytes did not show the same suppressive effect. These results suggested that activated H2(d) ALAK cells could specifically suppress the anti-H2(d) activity of the H2(b) splenocytes. Anti-tumor growth factor (TGF)beta antibody blockade did not diminish this suppressive effect of ALAK cells, suggesting that this activity is not dependent on TGF-beta secretion. ALAKs from gld (FasL mutant) mice suppressed the allo-responses as well as the wild-type ALAK cells. The ALAKs from pfp (perforin knockout) mice did not completely block the inhibitory effect, which suggested that the suppressive effect of the allogeneic ALAK cells could be partially caused by perforin-mediated killing. We further demonstrated that donor ALAK cells could promote engraftment by suppressing host alloreactive responses in a nonmyeloablative allogeneic BMT model. These studies suggest that activated donor NK cells specifically suppress the alloreactive cells and provide a promising way to promote donor engraftment without involving systemic and nonspecific suppression of the immune system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1523-6536
pubmed:author
pubmed:copyrightInfo
Copyright 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
772-81
pubmed:meshHeading
pubmed-meshheading:20197103-Animals, pubmed-meshheading:20197103-Antibodies, pubmed-meshheading:20197103-Bone Marrow Transplantation, pubmed-meshheading:20197103-CD4-Positive T-Lymphocytes, pubmed-meshheading:20197103-CD8-Positive T-Lymphocytes, pubmed-meshheading:20197103-Cell Count, pubmed-meshheading:20197103-Cell Proliferation, pubmed-meshheading:20197103-Cytotoxicity, Immunologic, pubmed-meshheading:20197103-Female, pubmed-meshheading:20197103-Graft Survival, pubmed-meshheading:20197103-H-2 Antigens, pubmed-meshheading:20197103-Interleukin-2, pubmed-meshheading:20197103-Isoantigens, pubmed-meshheading:20197103-Killer Cells, Natural, pubmed-meshheading:20197103-Lymphocyte Activation, pubmed-meshheading:20197103-Lymphocyte Culture Test, Mixed, pubmed-meshheading:20197103-Mice, pubmed-meshheading:20197103-Mice, Inbred BALB C, pubmed-meshheading:20197103-Mice, Inbred C3H, pubmed-meshheading:20197103-Mice, Inbred C57BL, pubmed-meshheading:20197103-Mice, Knockout, pubmed-meshheading:20197103-Pore Forming Cytotoxic Proteins, pubmed-meshheading:20197103-Spleen, pubmed-meshheading:20197103-T-Lymphocytes, pubmed-meshheading:20197103-T-Lymphocytes, Cytotoxic, pubmed-meshheading:20197103-Transforming Growth Factor beta, pubmed-meshheading:20197103-Transplantation, Homologous, pubmed-meshheading:20197103-Transplantation Immunology
pubmed:year
2010
pubmed:articleTitle
Activated allogeneic NK cells as suppressors of alloreactive responses.
pubmed:affiliation
Laboratory of Cellular and Molecular Tumor Immunology, Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, First Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't