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Relevant bibliographies by topics / Interferonγ-Lymphocytes

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Journal articles

Academic literature on the topic 'Interferonγ-Lymphocytes'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Interferonγ-Lymphocytes"

1

Nie, Bo, Xue Li, Yi Wei, et al. "Xianfanghuomingyin, a Chinese Compound Medicine, Modulates the Proliferation and Differentiation of T Lymphocyte in a Collagen-Induced Arthritis Mouse Model." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/6356871.

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In traditional Chinese medicine (TCM), xianfanghuomingyin (XFHM) is used to treat autoimmune diseases, including rheumatoid arthritis (RA). Here, we studied the mechanisms underlying its treatment effects, especially its anti-inflammatory effects in a collagen-induced arthritis (CIA) mouse model. We found that cartilage destruction and pannus formation were alleviated by treatment with XFHM. The abnormal differentiation of Th1 and Th17 cells was downregulated significantly by XFHM, and Th2 and Treg cells were upregulated. Moreover, the expression levels of specific cytokines and transcription

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2

Zeng, Defu, Sussan Dejbakhsh-Jones, and Samuel Strober. "Granulocyte Colony-Stimulating Factor Reduces the Capacity of Blood Mononuclear Cells to Induce Graft-Versus-Host Disease: Impact on Blood Progenitor Cell Transplantation." Blood 90, no. 1 (1997): 453–63. http://dx.doi.org/10.1182/blood.v90.1.453.

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Abstract The feasibility of transplanting peripheral blood mononuclear cells (PBMC) from granulocyte colony-stimulating factor (G-CSF)–treated normal human donors to myeloablated allogeneic hosts has been demonstrated recently. The current work examined the ability of recombinant G-CSF to alter peripheral blood T-cell function and graft-versus-host disease (GVHD) in a murine model of allogeneic G-CSF–mobilized PBMC transplantation. Administration of recombinant G-CSF to C57BL/Ka mice markedly increased the capacity of PBMC to reconstitute lethally irradiated syngeneic hosts. T- and B-lineage l

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3

Zeng, Defu, Sussan Dejbakhsh-Jones, and Samuel Strober. "Granulocyte Colony-Stimulating Factor Reduces the Capacity of Blood Mononuclear Cells to Induce Graft-Versus-Host Disease: Impact on Blood Progenitor Cell Transplantation." Blood 90, no. 1 (1997): 453–63. http://dx.doi.org/10.1182/blood.v90.1.453.453_453_463.

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The feasibility of transplanting peripheral blood mononuclear cells (PBMC) from granulocyte colony-stimulating factor (G-CSF)–treated normal human donors to myeloablated allogeneic hosts has been demonstrated recently. The current work examined the ability of recombinant G-CSF to alter peripheral blood T-cell function and graft-versus-host disease (GVHD) in a murine model of allogeneic G-CSF–mobilized PBMC transplantation. Administration of recombinant G-CSF to C57BL/Ka mice markedly increased the capacity of PBMC to reconstitute lethally irradiated syngeneic hosts. T- and B-lineage lymphocyte

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4

Zhang, Dazhi, Yong Liu, Min Shi, et al. "Autocrine, Not Paracrine, Interferon-Gamma Gene Delivery Enhances Ex Vivo Antigen-Specific Cytotoxic T Lymphocyte Stimulation and Killing." Journal of Biomedicine and Biotechnology 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/270985.

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The adoptive transfer of antigen-specific cytotoxic T lymphocytes (CTL) shows promise in the treatment of cancer and infectious diseases. We utilize adeno-associated virus-(AAV-) based antigen gene-loaded dendritic cells (DCs) to stimulate such antigen-specific CTL. Yet further improvements in CTL stimulation and killing may result by gene delivery of various Th1-response interferons/cytokines, such as interferonγ(IFN-γ), as the delivered gene can continuously produce that interferon. However which immune cell type should optimally express IFN-γis unclear as the phenotypes of both DC and T cel

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5

Berrebi, Dominique, Stefano Bruscoli, Nicolas Cohen, et al. "Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10." Blood 101, no. 2 (2003): 729–38. http://dx.doi.org/10.1182/blood-2002-02-0538.

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Glucocorticoids and interleukin 10 (IL-10) prevent macrophage activation. In murine lymphocytes, glucocorticoids induce expression of glucocorticoid-induced leucine zipper (GILZ), which prevents the nuclear factor κB (NF-κB)–mediated activation of transcription. We investigated whether GILZ could account for the deactivation of macrophages by glucocorticoids and IL-10. We found that GILZ was constitutively produced by macrophages in nonlymphoid tissues of humans and mice. Glucocorticoids and IL-10 stimulated the production of GILZ by macrophages both in vitro and in vivo. Transfection of the m

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6

Kapranov, NM, VG Savchenko, LA Kuzmina, et al. "Alterations of Multipotent Mesenchymal Stromal Cells Induced by Interaction with Allogeneic Lymphocytes In Vitro." June 8, 2017. https://doi.org/10.19070/2328-3548-1700042.

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Multipotent mesenchymal stromal cells (MSCs) are widely used for cell therapy. Treatment with interferon-γ (IFNγ) increases the immunomodulating properties of MSCs. When administered intravenously, MSCs interact with lymphocytes. It is impossible to follow the fate of MSCs in the recipient organism. The aim of this study was to investigate the properties of MSCs after their interaction with lymphocytes in vitro. Bone marrow MSCs were co-cultured for 4 days with activated and non-activated lymphocytes. A portion of the MSCs was pretreated with IFNγ. HLA-DR expression on the MSCs increased when

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7

Berrebi, Dominique, Stefano Bruscoli, Nicolas Cohen, et al. "Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10." December 31, 2002. https://doi.org/10.1182/blood-2002-02-0538.

Full text

Abstract:

Glucocorticoids and interleukin 10 (IL-10) prevent macrophage activation. In murine lymphocytes, glucocorticoids induce expression of glucocorticoid-induced leucine zipper (GILZ), which prevents the nuclear factor κB (NF-κB)–mediated activation of transcription. We investigated whether GILZ could account for the deactivation of macrophages by glucocorticoids and IL-10. We found that GILZ was constitutively produced by macrophages in nonlymphoid tissues of humans and mice. Glucocorticoids and IL-10 stimulated the production of GILZ by macrophages both in vitro and in vivo. Transfection of the m

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