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Table 1 Diseases in which tumor necrosis factor (TNF) blockade causes exacerbation

From: Multiple roles for tumor necrosis factor-α and lymphotoxin α/β in immunity and autoimmunity

Disease Intervention Result Mechanism References
1. Multiple sclerosis Anti-TNF, soluble TNFR Increase in CNS lesions and disease activity ? T-cell activation [1, 2]
2. Experimental allergic encephalomyelitis (EAE) TNF-α null mutation exacerbation of EAE Failure of usual regression of T-cell reactivity; prolonged ? T-cell activation [3]
3a. Murine 'lupus' in (NZB×NZW)F1 mice TNF administration (adult) 3–4 month delay in disease onset ? Inhibition of T-cell activation [4]
3b. Murine 'lupus' in (NZB×NZW)F1 mice Anti-TNF administration (adult) Earlier disease onset with increased severity ? T-cell activation [5]
3c. Murine 'lupus' in (NZB×NZW)F1 mice Heterozygous TNF null mutant Earlier disease onset with increased severity ? T-cell activation [6]
3d. Murine 'lupus' in (NZB×NZW)F1 mice Anti-IL-10 administration (adult) Delayed onset and decreased severity Increase in endogenous TNF, leading to decreased T-cell activation [5]
4a. Type 1 diabetes mellitus in (NOD) mice TNF i.p. in adult mice Delayed onset, decreased incidence of diabetes ? Inhibition of T-cell activation [7]
4b. Type 1 diabetes mellitus in (NOD) mice Anti-TNF in adult mice Variable, earlier onset with increased incidence ? T-cell activation [8]
  1. CNS, central nervous system; i.p., intraperitoneally; NOD, nonobese diabetic; TNFR, TNF receptor.