Standard labs can't tell mechanistically distinct conditions apart. Our Deep Immune Profile fills in what conventional panels miss.
We coordinate blood draws at multiple timepoints and running a set of advanced assays to build a mechanistic picture of a patient’s immune state.
High-dimensional flow cytometry, single-cell RNA sequencing, and single-cell ATAC-seq. T-cell subset skewing, monocyte activation states, NK cell phenotypes, regulatory deficits, and exhaustion signatures.
Plasma proteomics (thousands of proteins), clinically validated cytokine panel, type I interferon signature, complement pathway evaluation, and proteome-wide autoantibody discovery.
Whole genome sequencing and T-cell/B-cell repertoire sequencing. Inborn errors of immunity, pharmacogenomic variants, and clonal expansions suggesting antigen-driven autoimmune reactivity.
Plasma metabolomics, mitochondrial function testing, cell-free DNA methylation sequencing, and microbiome shotgun sequencing. Bioenergetic reserve, tissue-of-origin injury signals, and microbiome composition.
We organize thousands of data points into five immune circuits. Each one represents a different way your immune system can malfunction. This is what makes it possible to see why two patients with the same diagnosis can need very different treatments.
Your immune system's first responders (monocytes, macrophages) are stuck in overdrive. Instead of calming down after a threat, they keep causing tissue damage through persistent inflammatory signaling.
Your interferon- or T cell-driven immune response is misdirected, attacking your own tissues. This is the pattern behind many classic autoimmune conditions where the immune system loses the ability to tell self from threat.
Your B cells are producing antibodies that target your own body. These antibodies form complexes that deposit in tissues, triggering inflammation and organ damage.
Your immune system's "brakes" (regulatory T cells, gut microbiome signals, tissue repair pathways) aren't working properly. Without them, inflammation continues even after the original trigger is gone.
Your immune system's fighter cells are burned out or misfiring, often because of lingering viral infections, overactive mast cells, or clotting abnormalities tied to immune dysfunction.
The profiling readout maps directly to rule-in / rule-out therapeutic decisions. Each circuit and overlay points to a specific class of interventions your physician can evaluate.
| Circuit / Overlay | Potential Interventions to Consider (Examples) |
|---|---|
| A – Innate | IL-1/IL-6/TNF inhibitors; colchicine; NLRP3 inhibitors |
| B – IFN / T cell | Anifrolumab; JAK inhibitors; anti-IL-12/23; anti-IL-17 |
| C – Humoral | Rituximab; BAFF/complement-targeted agents; plasmapheresis |
| D – Regulatory | Low-dose IL-2; microbiome-directed Treg induction |
| E – Effector-stress | Mast-cell stabilizers; antivirals; complement inhibitors |
| Z1 – Genetic | Variant-specific targeted therapy |
| Z3 – Metabolic | mTOR modulators; NAD+ precursors; CoQ10 adjuncts |
| Z4 – Tissue | Organ-protective strategies; cfDNA monitoring |
Each engagement runs in analytical cycles: measure, synthesize, inform. Your care team adjusts based on real data, not guesswork. And because each cycle is structured like a protocol, you can actually tell whether something worked or didn’t.
Start with a free case assessment. We’ll review your situation and determine if Arden’s approach is right for your case.
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