Interferon-gamma suppresses B cell stimulation factor (BSF-1) induction of class II MHC determinants on B cells.

Mond, James J.; Carman, Julie A.; Sarma, Chander; Ohara, Junichi; Finkelman, Fred D.

doi:10.4049/jimmunol.137.11.3534

Cited by 120 publications

(2 citation statements)

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“…Acquired resistance to L. major infection relies on the activation of CD4 + T cells, which leads to the production of large amounts of IFN-γ and this induces parasite killing by macrophages following nitric-oxide release (12)(13)(14). Though the killing of the parasite is mainly orchestrated by IFN-γ through direct macrophage activation (6)(7)(8), the direct inhibition of the IL-4 (15,16) and the reduction in clonal expansion of Th2 cells by is also important. In addition, direct mechanisms allowing IL-4 to inhibit IFN-γ-activity have been identified, including the direct inhibition of macrophage activation to eliminate intracellular amastigotes 18).…”

Section: Introductionmentioning

confidence: 99%

Measuring the Immune Memory Response of In Vitro Polarized Th1, Th2, and Th17 Cells in the Face of OVA TransgenicLeishmania major inMouse Model

Tedla,

Nahar,

Every

et al. 2024

Preprint

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Th1 and Th2 cytokines determine the outcome ofLeishmania majorinfection and immune protection depends mainly on memory T cells induced during vaccination. This largely hinges on the nature and type of memory T cells produced. In this study, transgenicLeishmania majorexpressing membrane associated ovalbumin (mOVA) and soluble ovalbumin (sOVA) are used as a model to study whether fully differentiated Th1/ Th2 &Th17 cells can recall immune memory and tolerate pathogen manipulation. Naïve OT-II T cells werein vitropolarised into Th1/Th2, and these cells were transferred adoptively into recipient mice. Following transferring the memory cells, recipient mice were challenged with OVA transgenicLeishmania majorand wild type parasite was used a control. Thein vitropolarised T helper cells continued to produce the same cytokine signatures after challenged by both forms of OVA-expressingLeishmania majorparasitesin vivo. This suggests antigen-experienced cells cells remain the same or unaltered in the face of OVA transgenicLeishmania major. Such ability of the antigen-experienced cells to remain resilient to manipulation by the parasite signifies that vaccines might be able to produce immune memory responses and withstand against the parasite immune manipulation and protect the host from infection.

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Section: Introductionmentioning

confidence: 99%

Measuring the Immune Memory Response of In Vitro Polarized Th1, Th2, and Th17 Cells in the Face of OVA TransgenicLeishmania major inMouse Model

Tedla,

Nahar,

Every

et al. 2024

Preprint

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show abstract

“…Although, the basis for these reciprocal effects of cytokines is unclear, transcriptional antagonism between IL-4 and IFN-␥ has been amply documented (Refs. [10][11][12][13][14][15][16]reviewed in Ref. 17).…”

mentioning

confidence: 99%

Paired Stat6 C-Terminal Transcription Activation Domains Required Both for Inhibition of an IFN-Responsive Promoter andTrans-Activation

Goenka

Youn

Dzurek

et al. 1999

The Journal of Immunology

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The cytokines IL-4 and IFN-γ exert biologically antagonistic effects that in part reflect opposing influences on gene transcription. While the molecular mechanisms for IL-4-mediated transcription activation have been extensively studied, little is known about molecular mechanisms required for IL-4 inhibition of IFN-γ signaling. We have investigated IL-4 inhibition of the IFN-γ-inducible promoter for IFN regulatory factor-1 (IRF-1). In a cell line with low endogenous Stat6, increasing levels of activated Stat6 at constant doses of IFN-γ and IL-4 leads to inhibition of the IRF-1 promoter. The Stat1-dependent IFN-γ activation sequence element of the IRF-1 promoter is a target for Stat6-mediated inhibition despite apparently normal Stat1 DNA binding. However, our data are inconsistent with competition between Stat1 and Stat6 for access to the IRF-1 IFN-γ activation sequence or for an essential coactivator as a mechanism for this Stat6-mediated inhibition. Instead, the data demonstrate that a threshold of Stat6 transcription activation domains is required for IL-4-dependent inhibition. The findings provide evidence of a novel mechanism in which the Stat6 transcription activation domains play a critical role in the IL-4-mediated inhibition of an IFN-γ-inducible promoter.

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Schwann cells co‐cultured with stimulated T cells and antigen express major histocompatibility complex (MHC) class II determinants without interferon‐γ pretreatment: synergistic effects of interferon‐γ and tumor necrosis factor on MHC class II induction

Kingston¹,

Bergsteinsdóttir

Jessen

et al. 1989

Eur J Immunol

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Schwann cells (SC) do not express major histocompatibility complex (MHC) class II antigens under normal culture conditions. SC can, however, be induced in vitro to express MHC class II molecules by exposure to high concentrations of interferon-gamma (IFN-gamma) and can present antigens to antigen-specific T cell lines. In the present study immunohistochemical labeling showed that most SC (greater than 90%) prepared from rat neonatal sciatic nerves expressed MHC class II molecules when cultured together with mycobacterial antigen and T cells, and as a consequence were able to function as antigen-presenting cells in lymphoproliferation assays, without requiring pretreatment with IFN-gamma. Antigen or T cells alone were ineffective in stimulating MHC class II expression and induction of class II molecules was MHC restricted, requiring the presence of syngeneic T cells. Addition of monoclonal antibody DB1, directed against IFN-gamma to co-cultures of SC and T lymphocytes stimulated with antigen, prevented the induction of MHC class II antigen on SC. When SC were incubated with recombinant (r)IFN-gamma alone, up to 50% of SC showed positive labeling for MHC class II antigen. This level of expression was enhanced to greater than 80% when recombinant tumor necrosis factor (rTNF) was also added. rTNF alone had no effect, and addition of DBI antibody inhibited the synergistic effects of rTNF on MHC class II expression. The effects of rIL 4 were also investigated but neither rIL 4 alone nor rIL 4 in combination with rIFN-gamma induced MHC class II expression by SC. These results show that in the presence of sensitized T lymphocytes and antigen, SC do not require pretreatment with exogenous rIFN-gamma to express MHC class II antigens and function as antigen-presenting cells. T cell-derived TNF and IFN-gamma appear to act as mediators of the T cell-induced expression of MHC class II by SC.

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Interferon-gamma suppresses B cell stimulation factor (BSF-1) induction of class II MHC determinants on B cells.

Cited by 120 publications

References 0 publications

Measuring the Immune Memory Response of In Vitro Polarized Th1, Th2, and Th17 Cells in the Face of OVA TransgenicLeishmania major inMouse Model

Measuring the Immune Memory Response of In Vitro Polarized Th1, Th2, and Th17 Cells in the Face of OVA TransgenicLeishmania major inMouse Model

Paired Stat6 C-Terminal Transcription Activation Domains Required Both for Inhibition of an IFN-Responsive Promoter andTrans-Activation

Schwann cells co‐cultured with stimulated T cells and antigen express major histocompatibility complex (MHC) class II determinants without interferon‐γ pretreatment: synergistic effects of interferon‐γ and tumor necrosis factor on MHC class II induction

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