Intracerebroventricular infusion of an anti-TNF antibody blocked depression-like behavior and reduced persistent pain.

Circulating TNF alpha was not detectable in rats injected with anti-TNF antibody before zymosan.

Although anti-TNF antibody did not affect the above responses, primary interactions are strongly inhibited in vivo.

This effect did not require cell to cell contact and could be blocked by a neutralizing anti-TNF antibody.

Pretreatment with anti-TNF antibodies does not affect pulmonary or renal c-jun expression or AP-1 binding activity post-partial hepatectomy.

This enhancing activity was due to TNF and not impurities in TNF preparations as anti-TNF antibodies abolished this phenomenon.

It is also suggested that selective blocking of soluble TNF may be a better therapeutic option than using anti-TNF antibodies.

No differences were found with this approach in animals treated with anti-FasL and anti-TNF antibodies alone or the combination of both.

This second peak required an intact protein synthesis and was prevented by anti-TNF antibodies, suggesting the dependency on LPS-induced synthesis of TNF.

These results suggest that anti-TNF antibody may be interfering with soluble cytokines rather than with cell surface TNF causing depletion of cell populations.

In a 21-day adjuvant arthritis model, the anti-TNF antibody did not inhibit the ankle swelling or the joint destruction, as assessed by histology or radiology.