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CCL3 — IL10

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CCL3 → IL10 (decreases) Lim et al., Am J Respir Crit Care Med 2000*
  Evidence: These data are in accordance with the other known antiinflammatory and protective functions of IL-10, which include its inhibition of the production of several proinflammatory cytokines and chemokines by AM, including TNF-alpha , IL-1beta , IL-6, macrophage inflammatory protein-1alpha , and IL-8 (20, 30).

Text-mined interactions from Literome

Olszyna et al., J Infect Dis 2000 (Endotoxemia) : Sixteen healthy subjects were intravenously injected with lipopolysaccharide (LPS), once with placebo and once with recombinant human interleukin (IL)-10 ( 25 microgram/kg ), to determine the effect of IL-10 on LPS induced production of macrophage inflammatory protein (MIP)-1alpha , MIP-1beta, and monocyte chemoattractant protein (MCP)-1 ... In whole blood in vitro, the IL-10 induced inhibition of MIP-1alpha and MIP-1beta release was equally potent in the presence or absence of an anti-tumor necrosis factor (TNF) antibody
Waehre et al., J Am Coll Cardiol 2003 (Coronary Artery Disease) : Our main findings were : 1 ) gene expression of several chemokines ( i.e., macrophage inflammatory protein [MIP ] -1alpha, MIP-1beta, and interleukin [ IL]-8 ) and chemokine receptors ( i.e., CC chemokine receptor [ CCR]1, CCR2, CCR4, and CCR5 ) was markedly increased among CAD patients compared with healthy control subjects ; 2 ) treatment with atorvastatin and simvastatin markedly reduced the mRNA levels of some of these chemokines ( i.e., MIP-1alpha, MIP-1beta, IL-8 ) and receptors ( i.e., CCR1 and CCR2 ), with the most pronounced effect in the atorvastatin group ; and 3 ) statin therapy reduced the spontaneous release of IL-8 and MIP-1alpha from PBMCs in CAD patients
Waehre et al., Thromb Haemost 2004 (Inflammation) : Furthermore, activated platelets released comparable amounts of PGE ( 2 ), suggesting that platelet derived PGE2 could interact with PBMC in co-cultures ; ( iv ) IL-10 inhibited the platelet inducing effect on IL-6, IL-8 and MIP-1alpha in PBMC, and notably, the addition PGE2 totally abolished this IL-10 effect suggesting that the suppressive effect of IL-10 on the plateletinduced activation of PBMC might at least partly involve PGE ( 2 ) related mechanisms
Kornfeld et al., J Clin Invest 2005 (Acquired Immunodeficiency Syndrome...) : This was followed by a significant increase in levels of IL-10 , whereas IFN-gamma gene upregulation was more transient, and levels of TNF-alpha and MIP-1alpha/beta transcripts did not increase in either blood or tissues
Kremlev et al., J Neuroimmunol 2005 : IL10 inhibited TNFalpha, MIP-1alpha, and RANTES release of LPS stimulated MG cells as well as TNFalpha, MIP-1alpha , and CXCR3 mRNA expression by HAPI cells after exposure to LPS ( P < 0.05 )
Boyd et al., J Immunol 2005 : The wild-type acylated toxin ( A-CyaA ) and nonacylated CyaA ( NA-CyaA ), but not CyaA with an inactive adenylate cyclase domain ( iAC-CyaA ), enhanced TLR-ligand induced IL-10 and inhibited IL-12, TNF-alpha, and CCL3 production by macrophages and DC
Fan et al., Immunology 2007 : LPS induced production of tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-10 and interferon-gamma-inducible protein-10 (IP-10); SA induced TNF-alpha, and IL-1beta production ; and GBS induced TNF-alpha, IL-6, IL-1beta, macrophage inflammatory protein-1alpha ( MIP-1alpha ) and keratinocyte chemoattract ( KC ) production were all decreased ( P < 0.05 ) in Galpha ( i2 ) ( -/- ) or Galpha ( i1/3 ) ( -/- ) mice compared with WT mice
Wang et al., Arthritis Rheum 2013 (Intervertebral Disc Degeneration...) : Tumor necrosis factor a- and interleukin-1ß dependent induction of CCL3 expression by nucleus pulposus cells promotes macrophage migration through CCR1
Berkman et al., J Immunol 1995 : Because monocytes and macrophages are capable of releasing the C-C chemokine, macrophage inflammatory protein-1 alpha ( MIP-1 alpha ), which is a potent chemoattractant for activated T cells, we studied the effects of IL-10 on the expression of MIP-1 alpha in these cells ... In monocytes, IL-10 induced inhibition of MIP-1 alpha was only partially accounted for by alterations in mRNA stability and was dependent on de novo protein synthesis
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