Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Association of B7-1 co-stimulation with the development of graft arterial disease. Studies using mice lacking B7-1, B7-2, or B7-1/B7-2.

The American journal of pathology - 1 Aug 2000

Furukawa Y, Mandelbrot D A, Libby P, Sharpe A H, Mitchell R N

Abstract excerpt

To investigate the roles of B7-1 and/or B7-2 co-stimulatory molecule in the development of graft arterial disease (GAD), major histocompatibility complex (MHC) class II-mismatched allograft hearts were transplanted into wild-type, B7-1(-/-), B7-2(-/-), or B7-1/B7-2(-/-) recipient mice. Grafts were explanted at 4 or 8 weeks and used for histological and immunohistochemical analyses, RNase protection assay, and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antigen-Presenting Cells
Share to B7-1 Antigen

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to B7-2 Antigen

Share to Chemokines

Share to Graft Rejection

Share to Heart Transplantation

Share to Histocompatibility Antigens Class II

Share to Transplantation, Homologous

Source

Open in PubMed Open full text

Identifiers

PMID: 10934151
DOI: 10.1016/S0002-9440(10)64559-2
PMCID: PMC1850132

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Association of B7-1 co-stimulation with the development of graft arterial disease. Studies using mice lacking B7-1, B7-2, or B7-1/B7-2.PMID 10934151Read ↗

Pancreatic expression of B7 co-stimulatory molecules in the non-obese diabetic mouse.Semantic proximity Read ↗

Kinetics of transplant arteriosclerosis in MHC-Class I mismatched and fully allogeneic mouse aortic allografts.Semantic proximity Read ↗

Distinct roles for B7-1 (CD-80) and B7-2 (CD-86) in the initiation of experimental allergic encephalomyelitis.Semantic proximity Read ↗

Cardiac allograft vasculopathy--the cellular attack.Semantic proximity Read ↗

Graded function of CD80 and CD86 in initiation of T-cell immune response and cardiac allograft survival.Semantic proximity Read ↗

Genetic background determines the requirement for B7 costimulation in induction of autoimmunity.Semantic proximity Read ↗

B cell phenotypes in baboons with pig artery patch grafts receiving conventional immunosuppressive therapy.Semantic proximity Read ↗

Studies Using Antigen-Presenting Cells Lacking Expression of Both B7-1 (CD80) and B7-2 (CD86) Show Distinct Requirements for B7 Molecules During Priming Versus Restimulation of Th2 But Not Th1 Cytokine ProductionSemantic proximity Read ↗

CD28-B7-mediated T cell costimulation in chronic cardiac allograft rejection: differential role of B7-1 in initiation versus progression of graft arteriosclerosis.Semantic proximity Read ↗

B7-1 or B7-2 is required to produce the lymphoproliferative phenotype in mice lacking cytotoxic T lymphocyte-associated antigen 4 (CTLA-4).Semantic proximity Read ↗

Gene expression profiling of allogeneic islet grafts in an experimental mouse model before rejection or tolerance phenotypes arise.Semantic proximity Read ↗

Acute cardiac allograft rejection in nitric oxide synthase-2(-/-) and nitric oxide synthase-2(+/+) mice: effects of cellular chimeras on myocardial inflammation and cardiomyocyte damage and apoptosis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.