Journal
JOURNAL OF IMMUNOLOGY
Volume 172, Issue 1, Pages 34-39Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.1.34
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Funding
- NHLBI NIH HHS [2R37 HL 56067] Funding Source: Medline
- PHS HHS [R01 34495] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL056067] Funding Source: NIH RePORTER
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Although B7 on APCs has a well-recognized role in T cell costimulation, little is known about the functional significance of constitutive and activation-induced B7 expression that also occurs on T cells. To analyze the role of B7 on T cells, B7-1/B7-2-deficient mice (B7 double knockout) and mice overexpressing B7-2 exclusively on T cells (B7-2 transgenic) were used as T cell donors for allogeneic transplant recipients, and graft-vs-host disease (GVHD) was assessed. B7 double-knockout T cells resulted in significant GVHD acceleration compared with wild-type T cells. Conversely, B7-2 transgenic donor T cells mediated reduced GVHD mortality compared with wild-type T cells. Data indicated that B7 expression on T cells down-regulated alloresponses through CTLA-4 ligation. This study is the first to provide definitive in vivo data illustrating the importance of T cell-associated B7 as a negative regulator of immune responses in a clinically relevant murine model of GVHD. The up-regulation of B7 on T cells maybe an important component of normal immune homeostasis.
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