Molecular focus in Tumour necrosis factor α andAnti-Tnf α therapy

Tumour necrosis factor α(TNFα) can induce tumour regression through the induction of cell death. The best-characterized functions of TNF are related to apoptosis and inflammation, but these are not the only ones. TNF is also involved in many diseases including malaria, AIDS and cancer. In the absence of TNF signalling, secondary lymphoid organs fail to develop properly, and this is at least partly due to a migration defect in follicular dendritic cells. Further studies using TNFR1/TNFR2 knock-out mice have suggested a neurotoxic role for TNFR1 versus a neuroprotective role of TNFR2. Now this is obvious that proinflammatory cytokines were present in the synovium and plasma of patients with RA. Tuberculosis testing has been recommended for patients commencing anti-TNF-α therapies. Whether an optimized version of any current injectable therapeutic will exhibit greater clinical efficacy alone or, in contrast, exhibit increased immunogenicity is unknown. In addition, the potential for adverse effects, such as activation of latent tuberculosis or increased incidence of cancer, is uncertain and must be addressed with any second generation protein-based therapy.