Interactive translational immunology reference
From immune circuit to clinical manifestation to treatment effect.
Explore the dominant cytokines, cells, signaling pathways, drug mechanisms and manifestation-specific therapeutic effects across major rheumatology–dermatology overlap diseases. Every tabular row carries an explicit evidence grade and source trail.
Immune-pathway intensity map
Maximum mechanistic significance (1–5) by condition and canonical pathway family. Unmapped axes remain unknown, not zero.
Selected condition pathway fingerprint
Relative importance of the strongest mapped canonical axes; unmapped axes remain explicitly unknown.
Evidence distribution
Evidence grades are reported separately for each construct so unlike rows are never pooled.
0Pathway rows
Condition library
Open a module for physiology, causal pathophysiology, manifestations, biomarkers and treatment map.
Immune pathways and cytokines by condition
Significance is a biologic synthesis, not a serum-cytokine ranking. Click any row for detailed rationale and sources.
Medication mechanisms and signaling consequences
Primary target, direct action and secondary immune effects are separated to reduce mechanistic overgeneralization.
Comparative benefit profile
Qualitative benefit magnitude for the manifestations named in each row.
How to interpret benefit
Cross-trial comparisons are intentionally ordinal, not a network meta-analysis.
A score applies only to the listed manifestations and disease context. A therapy may be transformative for one organ domain and ineffective—or harmful—for another. Endpoint definitions, background therapy, population enrichment and trial duration differ substantially.
Medication × condition × manifestation matrix
Click a row for endpoint interpretation, onset and caveats.
Manifestation × pathway evidence matrix
Cell intensity encodes relationship strength; the letter encodes pairwise evidence grade. Blank cells mean no relationship was mapped from the embedded synthesis.
Manifestation–pathway relationship table
Search, sort and export the pairwise map. Every row includes directness, strength, consistency and an evidence grade.
Ligand → receptor → kinase → transcription factor
JAK–STAT signal wiring
Ten canonical receptor-family routes. Select a route to inspect its receptor complex, kinase pairing, STAT usage and representative downstream program.
Interpretation boundary. No combined magnitude is calculated. The overlap row reports set membership only; it estimates no synergy, antagonism, dose response, tissue exposure, efficacy, or safety. Named JAK1/2/3 agents project to the atlas’s JAK-inhibitor class relation; deucravacitinib projects to its TYK2 entry. Unknown is not equivalent to unaffected.
Relational matrix workbench
Overlap and difference comparator
Inspect a focused pair or scan the complete cohort against the same fixed entity order. Every coordinate remains visible, and every view reports its denominator.
Direct evidenceExplicit zeroFiltered by evidenceUnknown / unmappedDerived relationship
Rows: entity A, entity B, shared, A-only, B-only. Click any cell for its evidence trail and provenance.ORDER: deterministic · CAMERA: orthographic · DEPTH: facet index
Pathways · 27
Treatments · 49
Features · 124
All 18 conditions remain in a frozen order. Scroll horizontally without changing the denominator.UNKNOWN ≠ ABSENT · DERIVED ≠ DIRECT
Antibody-defined endotypes
Dermatomyositis antibody association matrix
Direction and consistency of cohort-level associations. Marks describe enrichment, inverse association, or variability—not deterministic prediction for an individual.
Assay and population caveat. Commercial line/dot immunoassays can disagree with reference methods, especially for weak positives, and association strength varies by age, ancestry, referral setting, and ascertainment. Interpret antibody identity with the testing platform and the full phenotype.
Within-condition heterogeneity
Subtype navigator
Non-exclusive organizational phenotypes for each condition in the atlas. These labels overlap and are not a replacement for formal classification criteria.
Teaching controls
Generate a mechanism-focused quiz from the live dataset.
Question generation is deterministic from the embedded evidence table but not a validated assessment instrument. Use explanations to discuss why plausible distractors are wrong.
Suggested instructional sequence
A 30–45 minute small-group framework.
- Define normal tissue physiology and the failed homeostatic checkpoint.
- Trace the causal pathway flow rather than memorizing isolated cytokines.
- Contrast upstream targets, effector cytokines and intracellular signal inhibitors.
- Use the benefit matrix to expose organ-domain discordance.
- End with evidence-grade and trial-endpoint critique.
Quiz workspace
Choose a scope and start a quiz.
Evidence grading framework
A pragmatic hybrid of intervention evidence and mechanistic human validation.
Scope and limitations
Important boundaries for educational use.
Not medical advice. This atlas omits dosing algorithms, contraindication detail, pregnancy management, vaccination schedules and many rare therapies. “Pathway importance” is a structured synthesis, not a validated biomarker score. “Benefit” is ordinal and should not be used for indirect treatment ranking across trials.
- Rare-disease rows necessarily rely more on cohorts and case series.
- Off-label and investigational use is labeled in mechanism/caveat text.
- Regulatory status varies by country and can change after the evidence cutoff.
- Organ-threatening disease requires disease-specific guideline and specialist review.
Source library
Guidelines, pivotal trials, regulatory sources and mechanistic reviews used for the synthesis.