Simplified model of immune responses.
- Nury M. Steuerwald (337041)
- David M. Foureau (502758)
- H. James Norton (502759)
- Jie Zhou (28945)
- Judith C. Parsons (502760)
- Naga Chalasani (458664)
- Robert J. Fontana (502761)
- Paul B. Watkins (502762)
- William M. Lee (502763)
- K. Rajender Reddy (414631)
- Andrew Stolz (502764)
- Jayant Talwalkar (502765)
- Timothy Davern (502766)
- Dhanonjoy Saha (502767)
- Lauren N. Bell (502768)
- Huiman Barnhart (502769)
- Jiezhun Gu (502770)
- Jose Serrano (502771)
- Herbert L. Bonkovsky (210820)
Publication date
December 2013
DOIAbstract
<p>Immune stimuli trigger NFκB nuclear translocation and early/innate cytokine production (IL-1β, IL-6, TNF-α) by damaged tissue. If this early inflammatory state persists, it will activate adaptive immune processes favoring either cellular (T-box transcription factor TBX21 (e.g., T-bet)-dependent / TH1-type: IL-12p70, IFNγ, IL-2, IL-15) or humoral (Gata3-dependent /TH2-type: IL-4, IL-5, IL-13) responses. This inflammatory state may ultimately resolve itself by triggering anti-inflammatory processes (IL-10, IL-1ra). In the event of an unresolved inflammatory state, innate and anti-inflammatory processes synergize to evolve into RoRγt-dependent / TH17-type: IL-17 or IRF4-dependent TH9-type IL-9 adaptive immunity.</p
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