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- Table of Contents
Interactive map for innate immune activation, MAPK and NF-κB responses
Explore pathway targetsInteractive pathway map — select a highlighted node
High-confidence gene mappings from the native pathway map. Exact SKUs are retained where already validated; remaining targets open live catalog matches.
| Target | Role in pathway | Boster antibody route | Status |
|---|---|---|---|
| IL18 | Initiating cytokine | View live matches | Needs product selection |
| IL18R1 | Receptor signaling chain | View live matches | Needs product selection |
| MYD88 | Proximal adaptor | View live matches | Needs product selection |
| IRAK1 | Adaptor-associated kinase | View live matches | Needs product selection |
| TRAF6 | Signal-amplifying E3 ligase | View live matches | Needs product selection |
| IKBKB (IKK) | NF-κB activation | PA2036-1 | Exact SKU |
| NFKB1 | Inflammatory transcription | PA2111 | Exact SKU |
| RAF1 | MAPK branch | A00446-1 | Exact SKU |
| MAPK14 (p38) | Stress-activated kinase output | View live matches | Needs product selection |
| JUN (AP-1) | Inflammatory transcription | View live matches | Needs product selection |
IL-18 is an IL-1-family cytokine that signals through a heterodimeric receptor complex. Receptor engagement recruits MyD88 and IRAK-family proteins, then branches through TRAF6 into NF-κB and MAPK programs. The resulting transcriptional response supports inflammatory cytokine production and context-dependent IFN-γ biology.
IL-18R, MyD88, IRAK and TRAF6 establish the receptor-to-cytoplasm relay.
IKK activation releases NF-κB-dependent inflammatory transcription.
JNK, p38 and AP-1 broaden the response to stress and cytokine inputs.
Scale-test note: several labels on the source artwork are protein families or historical aliases. Only nodes with defensible human gene mappings are clickable.
IL-18 shares MyD88–IRAK–TRAF6 architecture with other IL-1-family and Toll-like receptor pathways. Downstream convergence on NF-κB, JNK and p38 means orthogonal controls are essential when assigning an observed response specifically to IL-18.
IL-18 can cooperate with additional cytokines to amplify IFN-γ-oriented responses.
Supports inflammatory mediator production through NF-κB and MAPK outputs.
Response strength depends on receptor expression and local inflammatory cues.
No. Pair cytokine measurement with receptor-proximal or downstream activation markers and a functional output.
IL-18BP is a soluble regulator that can reduce bioavailable IL-18 even when total IL-18 is elevated.