Which transcription factor complex is activated via Toll-like receptor signaling in response to GI microorganisms and is involved in pro-inflammatory cytokine production?

• A. STAT3
• B. NF-κB
• C. AP-1
• D. p53

Answer: (B)

When Toll-like receptors sense microbial components from GI organisms, the signaling cascades converge on NF-κB. In resting cells, NF-κB is kept inactive in the cytoplasm by IκB. TLR signaling activates the IKK complex, which phosphorylates IκB and marks it for degradation. Once IκB is removed, NF-κB translocates to the nucleus and drives transcription of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6, mounting the innate inflammatory response in the gut. While other factors like AP-1 can also be activated downstream, NF-κB is the central transcriptional regulator directly linked to TLR signaling and pro-inflammatory cytokine production in this context.