Discovering differential activation machinery of the Toll-like receptor 4 signaling pathways in MyD88 knockouts

To understand differential time activation of nuclear factor κB (NF-κB) and the temporal features of the downstream pro-inflammatory cytokines’ [tumour-necrosis-factor-α (TNF-α) and IP-10] mRNA levels in myeloid differentiation primary-response protein 88 (MyD88) knockouts (KOs), I developed a computational model of the TLR4 pathway. The result suggests that the late phase expression of NF-κB activity observed in MyD88 KOs is possibly due to a number of novel intermediates acting along the MyD88-independent pathway. I also simulate that the TNF-α levels will increase at a longer time in MyD88 KOs, not previously mentioned.