B7-H1, a third member of the B7 family, co-stimulates T-cell proliferation and interleukin-10 secretion

Dong, Haidong; Zhu, Gefeng; Tamada, Koji; Chen, Lieping

doi:10.1038/70932

Cited by 2,231 publications

(1,761 citation statements)

References 23 publications

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“…Similarly, injection of mAb to PD-1 [13] or PD-L1 [14] accelerated allograft rejection in immunosup-pressed recipients. However, although most studies indicate that the PD-1/PD-L1 pathway negatively regulates T cell activation and proliferation, there is evidence for a positive costimulatory effect of PD-L1 on TCR activation of naive murine T cells [3,15]. Here, we report data showing that both PD-1 and PD-L1 are essential for the induction and maintenance of allograft tolerance.…”

Section: Introductionmentioning

confidence: 75%

“…PD-1 has two ligands, PD-L1 (also known as B7-H1 or CD274), constitutively expressed by many tissues and upregulated on activation [3], and PD-L2 (also known as B7-DC or CD273), expressed primarily by activated DC and macrophages [4]. Upon ligation by either molecule, PD-1 recruits the SHP-1 and SHP-2 phosphatases to its ITSM, leading to dephosphorylation of effector molecules downstream of the TCR and the BCR, such as Syk and phosphoinositide 3-kinase (PI3K), as well as decreasing CD28-mediated activation of PI3K [5].…”

Section: Introductionmentioning

confidence: 99%

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Programmed cell death 1 (PD‐1) and its ligand PD‐L1 are required for allograft tolerance

2007

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Programmed cell death-1 (PD-1, CD279) and its widely expressed, inducible ligand, PD-L1 (CD274), together dampen T cell activation, but whether they are essential for allograft tolerance is unknown. We show, using gene-deficient mice and blocking mAbs in wild-type mice, that costimulation blockade is ineffectual in PD-1 -/-or PD-L1 -/-allograft recipients, or in wild-type allograft recipients treated with anti-PD-1 or anti-PD-L1 mAb. Alloreactive PD-1 -/-CD4 and CD8 T cells had enhanced proliferation and cytokine production compared to wild-type controls, and anergy could not be induced in PD-1-deficient CD4 T cells. We conclude that without inhibitory signals from PD-1 ligation, alloantigen-induced T cell proliferation and expansion cannot be regulated by costimulation blockade, and peripheral tolerance induction cannot occur.

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Section: Introductionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Programmed cell death 1 (PD‐1) and its ligand PD‐L1 are required for allograft tolerance

2007

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“…9,10 PD-L1 is expressed constitutively on both hematopoietic cells (resting T cells, B cells, dendritic cell, macrophages, and regulatory T cells) and nonhematopoietic cells (parenchymal and endothelial cells) and is up-regulated to higher levels by inflammatory stimuli. [11][12][13][14] Peripheral tissue-specific PD-L1 expression indicates that it may have a key role in regulating or terminating immune responses in inflamed tissues. Previous studies from our laboratory and other groups have shown PD-L1 to play a critical function in peripheral immune tolerance as a negative regulator of T-cell responses.…”

mentioning

confidence: 99%

A Novel Function for Programmed Death Ligand-1

Jin

Chauhan

Annan

et al. 2011

The American Journal of Pathology

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Programmed death ligand-1 (PD-L1) plays a critical role in T-cell regulatory function. Here, we report a newly discovered effect of PD-L1 on angiogenesis. We demonstrate that PD-L1 and its receptor CD80, but not PD-1, are expressed by primary murine lung and heart vascular endothelial cells and the miscrovascular endothelial cell line (MS1) at both the mRNA and protein levels in vitro. The inhibition of PD-L1 or CD80 expression in MS1 cells, by small-interfering RNA transfection, led to a significant up-regulation of vascular endothelial growth factor receptor 2 expression and cell proliferation levels in MS1 cells. Furthermore, MS1 cells were found to have a significantly lower proliferation and vascular endothelial growth factor receptor 2 expression levels when they were co-cultured with PD-L1-expressing normal corneal epithelial cells, as compared to MS1 cells co-cultured with PD-L1 ؊/؊ corneal epithelial cells. In a sutureinduced corneal angiogenesis model, we observed a significantly higher level of angiogenic response in PD-L1 ؊/؊ knockout mice as compared to wild-type mice, although there was no significant difference in the expression of inflammatory cytokines (interleukin-1␣, interleukin-1␤, or tumor necrosis factor-␣) or the infiltration of innate immune cells (neutrophils and macrophages) between the two groups. We conclude that the expression of PD-L1 in both vascular endothelial cells and corneal epithelial cells regulates corneal angiogenesis.

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“…PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2), members of the B7 superfamily, are ligands for PD-1 [16][17][18][19]. Mouse (m) PD-L1 and PD-L2 share 38% amino acid identity and have extracellular Ig-like domains [4].…”

Section: Introductionmentioning

confidence: 99%

“…However, there is also evidence indicating that both PD-L1 and PD-L2 can costimulate T cell responses; i.e. in the presence of suboptimal TCR signals, PD-L1 or PD-L2 can stimulate increased proliferation and production of cytokines in vitro [16,19,20].…”

Section: Introductionmentioning

confidence: 99%

Paradoxical role of programmed death‐1 ligand 2 in Th2 immune responses in vitro and in a mouse asthma model in vivo

et al. 2004

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Programmed death-1 ligand 2 (PD-L2) is a ligand for programmed death-1 (PD-1), a receptor that plays an inhibitory role in T cell activation. Since previous studies have shown upregulation of PD-L2 expression by Th2 cytokines, and asthma is driven by a Th2 response, we hypothesized that PD-L2 might be involved in regulation of the immune response in this disease. We have found that lungs from asthmatic mice had sustained up-regulation of PD-1 and PD-L2, with PD-L2 primarily on dendritic cells. Although addition of PD-L2-Fc in vitro led to decreased T cell proliferation and cytokine production, administration of PD-L2-Fc in vivo in a mouse asthma model resulted in elevated serum IgE levels, increased eosinophilic and lymphocytic infiltration into bronchoalveolar lavage fluid, higher number of cells in the draining lymph nodes, and production of IL-5 and IL-13 from these cells. Although PD-1 was expressed on regulatory T cells, PD-L2-Fc did not affect regulatory T cell activity in vitro. This study provides in vivo evidence of an exacerbated inflammatory response following PD-L2-Fc administration and indicates a potential role for this molecule in Th2-mediated diseases such as asthma.

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B7-H1, a third member of the B7 family, co-stimulates T-cell proliferation and interleukin-10 secretion

Cited by 2,231 publications

References 23 publications

Programmed cell death 1 (PD‐1) and its ligand PD‐L1 are required for allograft tolerance

Programmed cell death 1 (PD‐1) and its ligand PD‐L1 are required for allograft tolerance

A Novel Function for Programmed Death Ligand-1

Paradoxical role of programmed death‐1 ligand 2 in Th2 immune responses in vitro and in a mouse asthma model in vivo

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