Immunological in vivo effects of B7-H1 deficiency

Bazhin, Alexandr V.; Ahn, Katharina von; Maier, Christoph A.; Soltek, Sabine; Serba, Susanne; Diehl, Linda; Werner, Jens; Karakhanova, Svetlana

doi:10.1016/j.imlet.2014.08.013

Cited by 4 publications

(16 citation statements)

References 72 publications

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“…Thus, we suppose that lack of the CD73 molecules may be compensated by appropriate changes in the expression of some stimulators on DC. In opposite to the B7H1 knockout model we did not detected differences in percentages of MDSC in the CD73 knockout mice [22].…”

Section: Discussioncontrasting

confidence: 87%

“…Concerning another type of innate immune cells -DC, we could not detect any changes in the total amount of cDC but sow a reduction of pDC as well as of the expression level of the costimulatory molecules CD80 and CD86 in transgenic mice. The same effects were seen by us in the healthy B7H1 knockout mice [22]. Thus, we suppose that lack of the CD73 molecules may be compensated by appropriate changes in the expression of some stimulators on DC.…”

Section: Discussionsupporting

confidence: 81%

“…It is surprising because as mentioned before the low amount of Ado (due to CD73 deficiency) should potentially lead to an increase in a frequency of these cells [21]. However, in our recent work with healthy B7H1 knockout mice, we also observed the decrease in NK cells' frequencies in transgenic mice [22]. The exact mechanism leading to this effect in both models is unclear.…”

Section: Discussionmentioning

confidence: 65%

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In Vivo Immunological Effects of CD73 Deficiency

Adam

Mathes

Isayev

et al. 2019

Cell Physiol Biochem

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Section: Discussioncontrasting

confidence: 87%

Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 65%

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In Vivo Immunological Effects of CD73 Deficiency

Adam

Mathes

Isayev

et al. 2019

Cell Physiol Biochem

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“…In the PD-1 and PD-L1 KO mice all cells are deficient for these molecules, so we cannot distinguish between direct or indirect effects on CD8 + T cells. For example, the absence of PD-L1 has a significant effect on the differentiation of myeloid cells (33). The following experiment was designed to test the direct influence of PD-L1 on the expansion of effector CD8 + T cells.…”

Section: Resultsmentioning

confidence: 99%

The PD-1/PD-L1 Pathway Affects the Expansion and Function of Cytotoxic CD8+ T Cells During an Acute Retroviral Infection

et al. 2019

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Cytotoxic CD8+ T lymphocytes (CTL) efficiently control acute virus infections but can become exhausted when a chronic infection develops. The checkpoint receptor PD-1 suppresses the functionality of virus-specific CD8+ T cells during chronic infection. However, the role of the PD-L1/PD-1 pathway during the acute phase of infections has not been well characterized. In the current study the effects of PD-1 or PD-L1 deficiency on the CD8+ T cell response against Friend retroviral (FV) infection of knockout mice was analyzed during acute infection. We observed an enhanced proliferation, functional maturation, and reduced apoptosis of effector CD8+ T cells in the absence of PD-1 or PD-L1. The knockout of PD-L1 had a stronger effect on the functionality of CD8+ T cells than that of PD-1. Augmented CTL responses were associated with an improved control of FV replication. The strong phenotype of FV-infected PD-L1 knockout mice was independent of the interaction with CD80 as an additional receptor for PD-L1. Furthermore, we performed a detailed analysis of the production of different granzymes in virus-specific CD8+ T cells and observed that especially the simultaneous production of multiple granzymes in individual T cells (multifunctionality) was under the control of the PD-1/PD-L1 pathway. The findings from this study allow for a better understanding of the development of antiviral cytotoxic immunity during acute viral infections.

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“…Shi et al find that expression of PD-1 is significantly enhanced in tumor and its adjacent tissues, promoting the apoptosis of CD8+T cells that are in contact with liver cancer cells [ 12 ]. Another study indicates that PD-1 inhibits antitumor immunity at CD8+T cell effector phase [ 13 ]. A study claims that activation of PD-1/PD-L1 signaling pathway leads to the formation of immunosuppressive tumor microenvironment that helps tumor cells evade immune surveillance and destruction, and blocking of PD-1/PD-L1 signaling pathway reverses tumor immune microenvironment [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

Elevated Expression of Programmed Death-1 and Programmed Death Ligand-1 Negatively Regulates Immune Response against Cervical Cancer Cells

Chen

Pang

et al. 2016

Mediators of Inflammation

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The present study is to measure the expression of programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1), as well as its clinical significance in cervical cancer patients. Our results showed that different T cell subsets in patients with cervical cancer had high expression of PD-1, and DCs had high expression of PD-L1. High expression of PD-1 on Treg cells in cervical cancer patients facilitated the production of TGF-β and IL-10 but inhibited the production of IFN-γ. Cervical cancer elevated the expression of PD-1 and PD-L1 in mRNA level. PD-1 expression in peripheral blood of cervical cancer patients was related with tumor differentiation, lymph node metastasis, and invasiveness. PD-1/PD-L1 pathway inhibited lymphocyte proliferation but enhanced the secretion of IL-10 and TGF-β in vitro. In summary, our findings demonstrate that elevated levels of PD-1/PD-L1, TGF-β, and IL-10 in peripheral blood of cervical cancer patients may negatively regulate immune response against cervical cancer cells and contribute to the progression of cervical cancer. Therefore, PD-1/PD-L1 pathway may become an immunotherapy target in the future.

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Immunological in vivo effects of B7-H1 deficiency

Cited by 4 publications

References 72 publications

In Vivo Immunological Effects of CD73 Deficiency

In Vivo Immunological Effects of CD73 Deficiency

The PD-1/PD-L1 Pathway Affects the Expansion and Function of Cytotoxic CD8+ T Cells During an Acute Retroviral Infection

Elevated Expression of Programmed Death-1 and Programmed Death Ligand-1 Negatively Regulates Immune Response against Cervical Cancer Cells

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