Source:http://linkedlifedata.com/resource/pubmed/id/20642683
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
2010-7-20
|
| pubmed:abstractText |
Sensitization to major histocompatibility complex (MHC) alloantigens is critical in transplantation rejection. The mechanism of sensitization to minor histocompatibility antigens (Mi-HAg) has not been thoroughly explored. We used a mouse model of allosensitization to Mi-HAg to study the Mi-HAg sensitization barrier in bone marrow transplantation (BMT). AKR mice were sensitized with MHC congenic Mi-HAg disparate B10.BR skin grafts. Adaptive humoral (B-cells) and cellular (T cells) responses to Mi-HAg are elicited. In subsequent BMT, only 20% of sensitized mice engrafted, while 100% of unsensitized mice did. In vivo cytotoxicity assays showed that Mi-HAg sensitized AKR mice eliminated CFSE labeled donor splenocytes significantly more rapidly than naïve AKR mice but less rapidly than MHC-sensitized recipients. Sera from Mi-HAg sensitized mice also reacted with cells from other mouse strains, suggesting that Mi-HAg peptides were broadly shared between mouse strains. The production of anti-donor-Mi-HAg antibodies was totally prevented in mice treated with anti-CD154 during skin grafting, suggesting a critical role for the CD154:CD40 pathway in B-cell reactivity to Mi-HAg. Moreover, anti-CD154 treatment promoted BM engraftment to 100% in recipients previously sensitized to donor Mi-HAg. Taken together, Mi-HAg sensitization poses a significant barrier in BMT and can be overcome with CD154:CD40 costimulatory blockade.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
1600-6143
|
| pubmed:author | |
| pubmed:issnType |
Electronic
|
| pubmed:volume |
10
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1569-79
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| pubmed:dateRevised |
2011-10-17
|
| pubmed:meshHeading |
pubmed-meshheading:20642683-Animals,
pubmed-meshheading:20642683-Antigens, CD40,
pubmed-meshheading:20642683-Bone Marrow Transplantation,
pubmed-meshheading:20642683-CD40 Ligand,
pubmed-meshheading:20642683-Child,
pubmed-meshheading:20642683-Graft Rejection,
pubmed-meshheading:20642683-Histocompatibility Testing,
pubmed-meshheading:20642683-Humans,
pubmed-meshheading:20642683-Immunity, Cellular,
pubmed-meshheading:20642683-Immunity, Humoral,
pubmed-meshheading:20642683-Isoantigens,
pubmed-meshheading:20642683-Lymph Nodes,
pubmed-meshheading:20642683-Lymphocyte Activation,
pubmed-meshheading:20642683-Major Histocompatibility Complex,
pubmed-meshheading:20642683-Male,
pubmed-meshheading:20642683-Mice,
pubmed-meshheading:20642683-Mice, Inbred AKR,
pubmed-meshheading:20642683-Mice, Inbred Strains,
pubmed-meshheading:20642683-Minor Histocompatibility Antigens,
pubmed-meshheading:20642683-Skin Transplantation,
pubmed-meshheading:20642683-Spleen,
pubmed-meshheading:20642683-Transplantation Chimera
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
Sensitization to minor antigens is a significant barrier in bone marrow transplantation and is prevented by CD154:CD40 blockade.
|
| pubmed:affiliation |
Institute for Cellular Therapeutics, University of Louisville, KY, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|