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CCL3 — IL7

Text-mined interactions from Literome

Llano et al., J Virol 2003 (HIV Infections) : Here, we show that IL-7 induced a dose dependent production of CCL3 ( MIP-1alpha ), CCL4 ( MIP-1beta ), and CCL5 ( RANTES ) in peripheral blood mononuclear cells ( PBMC ), ex vivo tonsil lymphoid tissue of HIV ( - ) individuals, and PBMC from HIV ( + ) individuals, suggesting that IL-7 may regulate beta-chemokine production in vivo
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
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