Cascades
Pick a lesson, then walk its steps. Each step opens the mechanism, what fails if that component is absent, and the clinical read-out. Draft extension lessons are labelled — not curated core.
Immunology Academy
Foundation is a navigable teaching scaffold; intermediate is an honest in-development scaffold over existing Mechanism lessons; advanced is labelled empty. Progress stays in this browser — not certification, not Gate C evidence coverage. Academy overview
Foundation: innate sensing → cytokines → inflammation
foundation · navigable scaffoldOne navigable beginner path through existing Mechanism lessons. Teaching simplifications are labelled; claim-level Gate C coverage is separate and may still be sparse.
Local quiz checks 0/6 · Lessons opened 0/3
- 1. not opened yetInnate sensing (TLR4 → NF-κB)
Trace LPS recognition to NF-κB-driven inflammatory transcription.
- 2. not opened yetCytokine networks (IL-6 chain)
Explain classical vs trans IL-6 signalling at a teaching level.
- 3. not opened yetInflammation effector (NLRP3 → IL-1β)
State the two-signal requirement for IL-1β release.
Intermediate: adaptive brakes, IFN sensing, type-2 effectors
intermediate · in development · scaffold onlyHonest scaffold over three existing Mechanism lessons (checkpoint, cGAS–STING, type-2). Not a finished intermediate curriculum — labelled in development; local quizzes only.
Local quiz checks 0/5 · Lessons opened 0/3 · In development
- 1. not opened yetCheckpoints at the synapse (CTLA-4 / PD-1)
Contrast CTLA-4 (priming) vs PD-1 (peripheral brake) as a teaching scaffold.
- 2. not opened yetCytosolic DNA → type I IFN (cGAS–STING)
Trace cytosolic DNA to IFNAR-driven ISG programmes at teaching depth.
- 3. not opened yetType-2 effectors (alarmins → asthma teaching path)
Place TSLP/IL-33 alarmins upstream of ILC2/Th2 teaching cascades.
Cytosolic DNA → type I IFN (cGAS–STING)
IFN teaching reuses the STING lesson. Exemplar IFN→SLE Gate C may still be scaffold — do not treat quiz completion as evidence approval.
Objectives
- Trace cytosolic DNA to IFNAR-driven ISG programmes at teaching depth.
- Link type I IFN amplification to BAFF / B-cell survival as a scaffold (not disease-complete).
- Name one IFNAR-targeted educational example without claiming CDS.
Teaching simplifications
- pDC and non-pDC IFN sources are collapsed for teaching.
- SLE biology is broader than the cGAS–STING spine shown here.
Graph concepts
Check understanding
Local practice only — not a credential, not SME sign-off, not evidence approval.
Advanced: systems integration (scaffold)
advanced · in development · scaffold onlyPlaceholder for multi-pathway integration lessons. No modules are navigable yet — labelled scaffold only, not a finished advanced course or certification.
Local quiz checks 0/0 · Lessons opened 0/0 · In development
cGAS–STING and type I interferon
How does a cell detect DNA in the wrong place, and why does that cause lupus?
Perturbation experiments
Break one component and follow the consequence chain to the clinical read-out.
Target: IFN → BAFF
- NETs and apoptotic debris deliver nucleic acid to pDCs (TLR7/9)
- pDCs release large amounts of IFN-α
- IFN induces BAFF on myeloid cells
- BAFF rescues autoreactive B cells from deletion
- More anti-dsDNA/immune complexes → more pDC activation (feed-forward loop)
Clinical read-out. Two drugs, two nodes of one loop: anifrolumab (IFNAR1) and belimumab (BAFF).
Target: TYK2
- TYK2 transduces IL-12, IL-23 and type I IFN
- Th17 maintenance (IL-23) falls
- Th1 (IL-12) and IFN responses fall
- IL-6 (JAK1/2) signalling largely spared
Clinical read-out. Deucravacitinib (allosteric TYK2) is approved for psoriasis, human TYK2 P1104A carriers are protected from several autoimmune diseases.