Gene interactions and pathways from curated databases and text-mining

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CCL3 — IFNG

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: CCL3 → IFNG (increases) D'Aversa et al., Am J Pathol 2002*
    Evidence: Treatment of cells with CD40L and IFN-gamma induced both protein and mRNA expression of MIP-1alpha. CD40L alone also induced MIP-1alpha expression, but treatment by CD40L and IFN-gamma potentiated the effect.

Text-mined interactions from Literome

Mohammed et al., Am J Respir Crit Care Med 1999 : IFN-gamma enhanced the BCG mediated MIP-1alpha and MCP-1 expression in a concentration dependent manner
Majka et al., J Clin Invest 1999 : We found that human CD34 ( + ) cells and CD34 ( + ) KIT ( + ) cells, which are enriched in myeloid progenitor cells, expressed and secreted the CCR5 ligands RANTES, MIP-1alpha , and MIP-1beta and that IFN-gamma stimulated expression of these chemokines
Tachimoto et al., J Allergy Clin Immunol 2000 : In contrast, IFN-gamma inhibited FcepsilonRI induced production of MIP-1alpha , IL-8, and GM-CSF
Rapisarda et al., Cell Immunol 2002 : Antagonistic effect of picolinic acid and interferon-gamma on macrophage inflammatory protein-1alpha/beta production
Ajuebor et al., Eur J Immunol 2004 (Disease Models, Animal...) : Correspondingly, hepatic IFN-gamma produced by the recruited CD4 ( + ) T cells was significantly reduced by CCL3/MIP-1alpha deficiency during Con A-induced hepatitis
Nath et al., Cancer Immunol Immunother 2006 (Adenocarcinoma...) : IFN-gamma co-stimulated and IL-4 suppressed MIP1alpha and beta induced cytotoxicity in PBM
Puliti et al., Microbes Infect 2006 (Arthritis...) : The worsening of sepsis and arthritis was associated with a significant increase in systemic and local production of IL-6, IL-1 beta, TNF-alpha, IL-10, macrophage inflammatory protein 1 alpha ( MIP-1alpha ), and MIP-2 and with a decrease in IFN-gamma production
Hedman et al., Clin Exp Immunol 2008 (Diabetes Mellitus, Type 1) : The percentages of CD4 ( + ) cells expressing CXC chemokine receptor 3 (CXCR3), CXCR6 and CCR5, and the secretion of interferon-gamma induced protein-10, monocyte chemoattractant protein-1, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta was lower among diabetics
Cassatella et al., Immunol Lett 1996 : Interferon-gamma inhibits the lipopolysaccharide induced macrophage inflammatory protein-1 alpha gene transcription in human neutrophils ... Lipopolysaccharide (LPS) is a potent inducer of macrophage inflammatory protein-1 alpha ( MIP-1 alpha ) production in human polymorphonuclear leukocytes ( PMN ), and it was recently shown that Interferon- gamma (IFN gamma) transiently inhibits MIP-1 alpha mRNA accumulation in LPS stimulated PMN ... IFN gamma did not affect MIP-1 alpha mRNA stability in LPS treated PMN, indicating that the cytokine does not regulate the LPS induced MIP-1 alpha gene expression through post-transcriptional events ... These results demonstrate that human neutrophils can actively transcribe the MIP-1 alpha gene, and that transcriptional inhibition is the mechanism whereby IFN gamma inhibits MIP-1 alpha gene expression in PMN
Lahrtz et al., Eur J Immunol 1997 (Meningitis, Viral) : To identify the chemotactic signals attracting the cells to the site of infection in the meninges, we measured the levels of two CXC chemokines, interferon-gamma (IFN-gamma) inducible protein (IP)-10 and monokine induced by IFN-gamma , four CC chemokines, monocyte chemotactic protein (MCP)-1, RANTES, macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta, as well as the cytokines interleukin (IL)-15 and IL-16 in the cerebrospinal fluid (CSF) of patients suffering from viral meningitis
Horton et al., J Immunol 1998 : We found that IL-10 and IFN-gamma independently inhibit HA-induced expression of macrophage inflammatory protein-1alpha ( MIP-1alpha ), MIP-1beta, and KC at both the mRNA and protein levels ... Whereas IL-10 inhibited most of the HA-induced chemokines tested, IFN-gamma selectively inhibited only MIP-1alpha , MIP-1beta, and KC
Flesch et al., Int Immunol 1998 : Release of infection triggered MIP-2, MIP-1alpha and KC was negatively regulated by IFN-gamma
Mohammed et al., J Infect Dis 1998 (Heart Failure...) : Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-gamma induced MIP-1alpha and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell derived C-C chemokines play a biologically important role in the recruitment of mononuclear cells to the pleural space