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).
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).
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.
Tumour necrosis factor alpha (TNF-alpha) is associated with clinical activity in relapsing-remitting multiple sclerosis (RRMS) and the development of progressive disease.
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.
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.