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CCL3 — IL2

Text-mined interactions from Literome

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
Sugimoto et al., J Exp Med 2004 (Bronchial Hyperreactivity...) : Newly polarized Th1 cells and IFN-gamma expressing Th1 cells, both of which express IL-18 receptor alpha chain strongly, produce IFN-gamma, IL-9, IL-13, granulocyte/macrophage colony stimulating factor, tumor necrosis factor alpha, regulated on activation, normal T cell expressed and secreted, and macrophage inflammatory protein 1alpha upon stimulation with Ag, IL-2 , and IL-18 in vitro
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
Minty et al., Eur Cytokine Netw 1997 : IL-13 does not significantly inhibit the IL-2 induced T lymphocyte production of IFN-gamma, RANTES, MIP-1 alpha or MIP-1 beta, nor that of perforin mRNA, as does IL-4