Update on the mechanisms of action of anti‑TNF-α antibodies and their clinical implications in inflammatory bowel disease

Possible under-treatment of women in Poland with Crohn’s disease: a subgroup analysis from a prospective multicenter study of the use of anti-TNFs

“…The final sample included 256 patients (113 women [44.1%] INTRODUCTION Anti-tumor necrosis factor (anti -TNF) antibodies improve the quality of life in patients with inflammatory bowel disease (IBD) 1 and likely modify the course of the disease via mucosal healing and a reduced rate of surgeries. [2][3][4][5][6][7] With an acceptable adverse event profile, TNF inhibitors can be considered the safest and most effective therapy for IBD. 8 The earlier in the course of the disease the anti -TNF treatment is introduced, the higher the probability of response and long -term remission.…”

No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis

“…Binding of antibodies to transmembrane TNF-α on target cells seems to be crucial for inducing complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and reverse signalling. However, these processes alone do not fully explain the mechanism of responses to anti-TNF-α therapy [4].…”

“…Curiously, treatment with TNF-α inhibitors does not significantly affect circulating TNF-α levels [5] and does not modulate the expression of TNF-α in the synovial tissue [6]. Therefore, there may exist alternative drivers of RA pathogenesis, which are affected by TNF-α inhibitors through as yet unidentified mechanisms [4].…”

PEG-<em>b</em>-(PELG-<em>g</em>-PLL) nanoparticles as TNF-&alpha; nanocarriers: potential cerebral ischemia/reperfusion injury therapeutic applications

“…It is generally accepted that TNF-α is an inflammatory cytokine involved in systemic inflammation and is one of the cytokines that make up the acute phase reaction. 18 It is produced chiefly by activated macrophages, neutrophils, mast cells, eosinophils, and neurons. TNF-α can mediate the ischemic tolerance in human stroke, whereby TNF-α aids in the preservation of mitochondrial membrane integrity, thereby blocking the onset of apoptosis.…”