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 | |
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] |