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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2005-1-24
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pubmed:abstractText |
Intervention in B7 (CD80/CD86)/B7-ligand (CD28/CTLA-4) pathways is an effective way of preventing unwanted immune responses, such as allograft rejection. Pregnancy maintenance represents maternal tolerance to the fetal allograft, which is accompanied by a type 2 helper cell (Th2) bias at the maternal-fetal interface. Here, the costimulatory signal of CD86 was selectively blocked, and that of CD80 was kept unimpaired by administration of anti-murine CD86 monoclonal antibody at the early gestational stage in abortion-prone CBA/JxDBA/2 matings and normal pregnant CBA/JxBALB/c matings. It was demonstrated that in vivo blockade of CD86 costimulation could suppress maternal immune attack to the fetus by shifting cytokines from Th1 predominance to Th2 bias at the maternal-fetal interface, and expanding peripheral CD4+CD25+ regulatory T cells, which play an important role in the development and maintenance of maternal-fetal tolerance. Furthermore, the expression of CD28 and its ligands CD80/CD86 on peripheral lymphocytes was down-regulated, whereas that of CTLA-4 was up-regulated, which might facilitate the suppressive effect of CD4+CD25+ regulatory T cells on the alloreactive T cells. The maternal-fetal immunotolerance induced by CD86 blockade decreased fetal resorption in CBA/JxDBA/2 matings, but did not affect normal pregnant CBA/JxBALB/c matings. These results suggest that selective blockade of CD86 costimulation leads to maternal immune tolerance to embryo antigen, and might contribute to a rational immunoregulatory regimen for recurrent spontaneous abortion.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Blocking,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Cd86 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0006-3363
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
72
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
338-45
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15456701-Abortion, Spontaneous,
pubmed-meshheading:15456701-Animals,
pubmed-meshheading:15456701-Antibodies, Blocking,
pubmed-meshheading:15456701-Antibodies, Monoclonal,
pubmed-meshheading:15456701-Antigens, CD,
pubmed-meshheading:15456701-Antigens, CD86,
pubmed-meshheading:15456701-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15456701-Cytokines,
pubmed-meshheading:15456701-Decidua,
pubmed-meshheading:15456701-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:15456701-Female,
pubmed-meshheading:15456701-Fetal Resorption,
pubmed-meshheading:15456701-Flow Cytometry,
pubmed-meshheading:15456701-Male,
pubmed-meshheading:15456701-Maternal-Fetal Exchange,
pubmed-meshheading:15456701-Membrane Glycoproteins,
pubmed-meshheading:15456701-Mice,
pubmed-meshheading:15456701-Mice, Inbred BALB C,
pubmed-meshheading:15456701-Mice, Inbred CBA,
pubmed-meshheading:15456701-Mice, Inbred DBA,
pubmed-meshheading:15456701-Placenta,
pubmed-meshheading:15456701-Pregnancy,
pubmed-meshheading:15456701-RNA, Messenger,
pubmed-meshheading:15456701-Receptors, Interleukin-2,
pubmed-meshheading:15456701-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15456701-Th1 Cells,
pubmed-meshheading:15456701-Th2 Cells
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pubmed:year |
2005
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pubmed:articleTitle |
Blockade of CD86 signaling facilitates a Th2 bias at the maternal-fetal interface and expands peripheral CD4+CD25+ regulatory T cells to rescue abortion-prone fetuses.
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pubmed:affiliation |
Laboratory of Reproductive Immunology, Institute of Obstetrics and Gynecology, Fudan University, Shanghai 200011, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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