Tumor Necrosis Factor Alpha Antagonists Inhibitors
Mostrando 1-4 de 4 artigos, teses e dissertações.
-
1. Evaluation of the effect of TNF-alpha inhibitors in the in vitro immune response to Mycobacterium tuberculosis antigens in patients with psoriasis / Avaliação do efeito do bloqueio de Fator de Necrose Tumoral alfa (TNF-) na resposta imune in vitro aos antígenos de Mycobacterium tuberculosis em pacientes com psoríase
O Fator de Necrose Tumoral-alfa (TNF-alfa) possui um importante papel na imunopatogênese da psoríase e agentes biológicos, como os inibidores de TNF-alfa, têm apresentado bons resultados no tratamento desta. No entanto, estes agentes foram associados ao aumento de casos de reativação de tuberculose entre os pacientes que os utilizaram. Este estudo foi
Publicado em: 2008
-
2. Photochemically enhanced binding of small molecules to the tumor necrosis factor receptor-1 inhibits the binding of TNF-α
The binding of tumor necrosis factor alpha (TNF-α) to the type-1 TNF receptor (TNFRc1) plays an important role in inflammation. Despite the clinical success of biologics (antibodies, soluble receptors) for treating TNF-based autoimmune conditions, no potent small molecule antagonists have been developed. Our screening of chemical libraries revealed that N-a
The National Academy of Sciences.
-
3. Inhibition of Tumor Necrosis Factor Alpha Alters Resistance to Mycobacterium avium Complex Infection in Mice
Increased production of tumor necrosis factor alpha (TNF-α) appears to play an important role in the progression of human immunodeficiency virus disease. One treatment strategy being explored is the use of TNF-α inhibitors. TNF-α also appears to be important in conferring resistance to infections, and the inhibition of this cytokine may exacerbate the eme
American Society for Microbiology.
-
4. Inhibition of human immunodeficiency virus type 1 replication in vitro by a novel combination of anti-Tat single-chain intrabodies and NF-kappa B antagonists.
Human immunodeficiency virus type 1 (HIV-1) Tat, an early regulatory protein that is critical for viral gene expression and replication, transactivates the HIV-1 long terminal repeat (LTR) via its binding to the transactivation response element (TAR) and, along with other cellular factors, increases viral transcription initiation and elongation. Tat also sup