The TNF-alpha (-308 bp) promoter/enhancer point mutation and two polymorphisms located within the first intron of the lymphotoxin (LT)-alpha gene showed neither significant allelic deviation for the patient group nor, after analysis of clinical characteristics such as blood counts, stable or progressive disease or response to therapy.
We conclude that a group of B-CLL patients with progressive disease have leukemic B cells able to exert in vitro a TNFalpha-mediated cytotoxicity, which is modulated by cytokines.
Tumour necrosis factor alpha (TNF-alpha) is associated with clinical activity in relapsing-remitting multiple sclerosis (RRMS) and the development of progressive disease.
Using a currently established encephalitic mouse model in which DENV infection causes progressive hunchback posture, limbic seizures, limbic weakness, paralysis, and lethality 7 days postinfection, we showed that TNF-α transgenic mice represented the progressive disease development and administration of neutralizing TNF-α Ab reduced dengue encephalitis and mortality.
In Cohort C, the increase in interleukin-8 and tumor necrosis factor-α (TNF-α) was significant in the PD group (p = 0.0063 and p < 0.001, respectively) but not in the SD + PR group (p = 0.67 and p = 0.15, respectively).
IL-2, IL-4, TNF-α, and IFN-γ levels in peripheral blood were significantly increased among the clinical responders (<i>p</i> < 0.05) while IL-6 and IL-10 were elevated among those with progressive disease (<i>p</i> < 0.05).