Decision letter for "Cell surface IL‐1α trafficking is specifically inhibited by interferon‐γ, and associates with the membrane via IL‐1R2 and GPI anchors"

2020 ◽  
Keyword(s):  
Cell Surface ◽  
Interferon Γ

Direct IFNluence of interferon-γ on proliferation and cell-surface antigen expression of non-small cell lung cancer cells

Lung Cancer ◽  
2000 ◽  
Vol 30 (3) ◽  
pp. 169-174 ◽  
Author(s):  
Tokujiro Yano ◽  
Kenji Sugio ◽  
Koji Yamazaki ◽  
Shinichiro Kase ◽  
Masafumi Yamaguchi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Surface ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Surface Antigen ◽  
Antigen Expression ◽  
Interferon Γ ◽  
Small Cell ◽  
Small Cell Lung ◽  
Surface Antigen Expression

Interferon-γ Upregulates CCR5 Expression in Cord and Adult Blood Mononuclear Phagocytes

Blood ◽  
1999 ◽  
Vol 93 (4) ◽  
pp. 1137-1144 ◽  
Author(s):  
Deepa Hariharan ◽  
Steven D. Douglas ◽  
Benhur Lee ◽  
Jian-Ping Lai ◽  
Donald E. Campbell ◽  
...  
Keyword(s):  
Cell Surface ◽  
Hiv Infection ◽  
Chemokine Receptors ◽  
Surface Expression ◽  
Interferon Γ ◽  
Mononuclear Phagocytes ◽  
Cell Surface Expression ◽  
Ccr5 Expression ◽  
Hiv Entry ◽  
Ifn Γ

Abstract The C-C chemokine receptors CCR5 and CCR3 are fusion coreceptors for human immunodeficiency virus (HIV) entry into macrophages. The regulation of their expression influences infectivity by HIV. We report here that interferon-γ (IFN-γ) a cytokine that has bidirectional effects on HIV infection of macrophages, significantly upregulated CCR5 and CCR3 cell surface expression in human mononuclear phagocytes isolated from placental cord blood and adult peripheral blood. Monocytes treated with IFN-γ showed increased chemotaxis to the CCR5 ligands macrophage inflammatory protein-1 (MIP-1) and MIP-1β, confirming the functional relevance of IFN-γ–induced CCR5 expression. However, IFN-γ suppressed HIV entry into macrophages. Interestingly, we demonstrated that IFN-γ inhibited cell surface expression of CD4, the major receptor for HIV. This finding may explain the suppressive effect of IFN-γ on HIV entry into macrophages, despite its enhancing effect on the expression of CCR5 and CCR3 by these cells. In addition, IFN-γ–induced secretion of C-C chemokines (RANTES, MIP-1, and MIP-1β) by mononuclear phagocytes may also suppress HIV entry into macrophages. These data provide further evidence for cytokine-mediated regulation of CCR5 expression and are consistent with a novel paradigm in which cytokines regulate HIV infection and leukocyte migration by reciprocal and opposing effects on the expression of CD4 and chemokine receptors.

From transcription to cell surface expression, the induction of MHC class II I-Aα by interferon-γ in macrophages is regulated at different levels

2001 ◽  
Vol 53 (2) ◽  
pp. 136-144 ◽  
Author(s):  
Martin Cullell-Young ◽  
Marta Barrachina ◽  
Carlos López-López ◽  
Eduard Goñalons ◽  
Jorge Lloberas ◽  
...  
Keyword(s):  
Cell Surface ◽  
Mhc Class Ii ◽  
Surface Expression ◽  
Class Ii ◽  
Interferon Γ ◽  
Cell Surface Expression ◽  
Different Levels

scholarly journals Induction of Lectin-like Transcript 1 (LLT1) Protein Cell Surface Expression by Pathogens and Interferon-γ Contributes to Modulate Immune Responses

2011 ◽  
Vol 286 (44) ◽  
pp. 37964-37975 ◽  
Author(s):  
Claire Germain ◽  
Anders Meier ◽  
Teis Jensen ◽  
Perrine Knapnougel ◽  
Gwenola Poupon ◽  
...  
Keyword(s):  
Cell Surface ◽  
Immune Responses ◽  
Surface Expression ◽  
Interferon Γ ◽  
Cell Surface Expression ◽  
Protein Cell

scholarly journals Cell Surface CD74–MIF Interactions Drive Melanoma Survival in Response to Interferon-γ

2015 ◽  
Vol 135 (11) ◽  
pp. 2775-2784 ◽  
Author(s):  
Keiji Tanese ◽  
Yuuri Hashimoto ◽  
Zuzana Berkova ◽  
Yuling Wang ◽  
Felipe Samaniego ◽  
...  
Keyword(s):  
Cell Surface ◽  
Interferon Γ

scholarly journals Fas Ligand Is Present in Human Erythroid Colony-Forming Cells and Interacts With Fas Induced by Interferon γ to Produce Erythroid Cell Apoptosis

Blood ◽  
1998 ◽  
Vol 91 (4) ◽  
pp. 1235-1242 ◽  
Author(s):  
Chun-Hua Dai ◽  
James O. Price ◽  
Thomas Brunner ◽  
Sanford B. Krantz
Keyword(s):  
Monoclonal Antibody ◽  
Cell Surface ◽  
Fas Ligand ◽  
Flow Cytometric Analysis ◽  
Interferon Γ ◽  
Cell Surface Receptor ◽  
Erythroid Cell ◽  
Erythroid Progenitors ◽  
Flow Cytometric ◽  
Fas Mrna

Abstract Interferon γ (IFNγ) inhibits the growth and differentiation of highly purified human erythroid colony-forming cells (ECFCs) and induces erythroblast apoptosis. These effects are dose- and time-dependent. Because the cell surface receptor known as Fas (APO-1; CD95) triggers programmed cell death after activation by its ligand and because incubation of human ECFCs with IFNγ produces apoptosis, we have investigated the expression and function of Fas and Fas ligand (FasL) in highly purified human ECFCs before and after incubation with IFNγ in vitro. Only a small percentage of normal human ECFCs express Fas and this is present at a low level as detected by Northern blotting for the Fas mRNA and flow cytometric analysis of Fas protein using a specific mouse monoclonal antibody. The addition of IFNγ markedly increased the percentage of cells expressing Fas on the surface of the ECFCs as well as the intensity of Fas expression. Fas mRNA was increased by 6 hours, whereas Fas antigen on the cell surface increased by 24 hours, with a plateau at 72 hours. This increase correlated with the inhibitory effect of IFNγ on ECFC proliferation. CH-11 anti-Fas antibody, which mimics the action of the natural FasL, greatly enhanced IFNγ-mediated suppression of cell growth and production of apoptosis, indicating that Fas is functional. Expression of FasL was also demonstrated in normal ECFCs by reverse transcriptase-polymerase chain reaction and flow cytometric analysis with specific monoclonal antibody. FasL was constitutively expressed among erythroid progenitors as they matured from day 5 to day 8 and IFNγ treatment did not change this expression. Apoptosis induced by IFNγ was greatly reduced by the NOK-2 antihuman FasL antibody and an engineered soluble FasL receptor, Fas-Fc, suggesting that Fas-FasL interactions among the ECFCs produce the erythroid inhibitory effects and apoptosis initiated by IFNγ.

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