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Table 2 Complex relation between TNF and type I IFN in murine studies

From: Type I IFN and TNFα cross-regulation in immune-mediated inflammatory disease: basic concepts and clinical relevance

Cross- regulation Cell type Activation state Experimental model Results Reference
IFN ↑ TNF ↓ Embryonic fibroblasts (MEF) and macrophages p38 MAPK stimulus In vitro stimulation with IFNβ and p38 MAPK stimulus simultaneously In the presence of a p38 MAPK stimulus, IFNβ induces - via STAT1 activation - TTP, which destabilizes mRNA of several proinflamatory genes including TNFα [16]
  Macrophages IFNγ and LPS Priming by IFNγ, stimulation by LPS in the presence of IFNβ-EF supernatant IFNβ suppressed LPS/IFNγ induced TNFα production [26]
  Synovial tissue CIA Daily treatment of CIA using recombinant IFNβ injection (7 days) FNβ treatment reduced TNFα production in the synovial tissue [28]
IFN ↑ TNF ↑ Macrophages Healthy In vitro stimulation with IFNβ IFNβ mediated upregulation of TNF mRNA [18]
IFN ↓ TNF ↑ Macrophages LPS and IFNγ EAE in IFNβ KO mice Increased TNFα production compared with wild-type controls [23]
  Spleen-derived macrophages LPS and IFNγ Cells isolated from IFNβ-deficient mice. Priming by IFNγ with subsequent stimulation with LPS Increased TNFα production compared with control mice [24]
  Synovial tissue CIA CIA in IFNβ-deficient mice Increased TNFα production in synovial of arthritic IFNβ-deficient mice [24]
IFN ↓ TNF ↓ Liver TNFα-induced lethal shock IFNAR1 or IFNβ KO mice Lack of type I IFN signaling protects against TNFα-induced inflammation [25]
TNF↓ IFN ↑ Serum Poly I:C NZB/W mouse (defect in TNF) injected with poly I:C NZB/W mice produce more poly I:C- induced IFNα [22]
  1. CIA, collagen-induced arthritis; EAE, experimental autoimmune encephalomyelitis; EF, expressing fibroblasts; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; MEF, muse embryonic fibroblast; poly I:C, polyinosinic-polycytidylic acid; STAT, signal transducers and activators of transcription; TTP, tristetraprolin.