Skip to main content

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.