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CCL4L2 — TNF

Text-mined interactions from Literome

Bliss et al., J Immunol 1999 (Toxoplasmosis) : These results establish that T. gondii possesses the ability of driving neutrophil proinflammatory cytokine production, and they suggest that parasite induced MIP-1 alpha and MIP-1 beta partly results from autocrine stimulation through TNF-alpha
Brice et al., J Acquir Immune Defic Syndr 2000 : Results of these studies show that the anti-viral resistance induced by activation of CD4+ T cells with anti-CD3 + anti-CD28 is primarily conferred by the synthesis of tumor necrosis factor-alpha (TNF-alpha), and highlight a unique regulatory role for TNF-alpha in regulating synthesis of MIP-1alpha, MIP-1beta , and regulated-on-activation normal T-expressed and secreted cells, which contributes to this state of antiviral resistance to R5-tropic strains of HIV/SIV
Wong et al., Allergy 2006 : Either SCF or TNF-alpha could induce release from HMC-1 cells of interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1, regulated upon activation normal T-cell expressed and secreted ( RANTES ), and I-309, while SCF and TNF-alpha induced release of macrophage inflammatory protein (MIP)-1beta and interferon-gamma-inducible protein-10 (IP-10), respectively
Sethu et al., PloS one 2010 (Disease Models, Animal...) : Similarly TNFalpha caused an increase in the serum levels of IL-6, MIP-1alpha and MIP-1beta : this increase in cytokine/chemokine levels was inhibited in mice where PLD1 had been silenced