Learn how immune pathways work, why they matter for your treatment, and how PathwayBio testing can help you find the right medication for your body.
Think of your immune system like a highway network in your body. Just as roads connect different cities, immune pathways are the routes that inflammatory signals travel through your body.
When you have an autoimmune disease, certain "highways" become overactive—sending too many inflammatory signals that attack your own tissues instead of protecting you from infections. Different people use different highways (pathways), which is why the same medication works great for some patients but doesn't help others at all.
Current treatment is like closing random highways and hoping you picked the right one. PathwayBio testing shows you which highways are actually causing the traffic jam in your immune system—so you and your doctor can block the right ones from the start.
This means you skip months or years of trying medications that were never going to work for YOUR immune system.
Your immune cells communicate using molecules called cytokines—think of these like text messages between cells. When immune cells send certain cytokine messages, they activate specific pathways that cause inflammation.
Immune cells send cytokine "texts" like IL-23, TNF-α, or IL-17 to activate inflammation.
These messages travel specific routes (pathways) through your immune system to cause damage.
Medications block specific cytokine messages—but only if you're using the right pathway.
Understanding which pathway drives YOUR intestinal inflammation
What it does: This pathway drives inflammation deep in the intestinal wall, causing ulcers, strictures, and fistulas. It's the dominant pathway in about 40-50% of Crohn's patients.
Key markers we test: IL-23, IL-17A, IL-17F, IL-22, IL-21
If this is YOUR pathway, these drugs work best: Skyrizi (risankizumab), Tremfya (guselkumab), Stelara (ustekinumab)
If this is NOT your pathway: These expensive biologics likely won't help you, and you'll waste 6-12 months finding out.
What it does: TNF-α is a "master switch" cytokine that amplifies inflammation throughout the gut. Common in patients with extensive disease or extraintestinal manifestations.
Key markers we test: TNF-α, soluble TNF receptors
If this is YOUR pathway: Humira (adalimumab), Remicade (infliximab), Cimzia (certolizumab)
Why some patients fail TNF blockers: Their disease isn't TNF-driven—it's IL-23 or another pathway. Testing tells you this upfront.
What it does: Drives transmural inflammation and granuloma formation. Often seen with stricturing or penetrating disease patterns.
Key markers we test: IL-12, IFN-γ, IL-2
Treatment considerations: May respond to Stelara (blocks IL-12/23) or combination therapy approaches.
IL-6: Amplifies inflammation and correlates with disease activity
IL-1β: Activates inflammasome, drives acute inflammation
IL-8: Recruits neutrophils to inflamed tissue
TGF-β: Associated with fibrosis and stricture formation
IL-10: Anti-inflammatory; low levels worsen disease
Understanding which pathway drives YOUR neuroinflammation
What it does: B-cells produce antibodies that attack myelin (the protective coating on nerves) and present antigens that activate other immune cells. Dominant in relapsing-remitting MS.
Key markers we test: CD19+ B-cells, memory B-cells, BAFF/BLyS, CXCL13
If this is YOUR pathway: Ocrevus (ocrelizumab), Kesimpta (ofatumumab), Rituxan (rituximab)
Why this matters: B-cell depleting drugs are highly effective—but only if B-cells are driving YOUR MS.
What it does: Th17 cells cross the blood-brain barrier and recruit inflammatory cells to attack myelin. Associated with more aggressive, inflammatory MS phenotypes.
Key markers we test: IL-17A, IL-17F, IL-23, IL-21, IL-22
Treatment considerations: May respond better to Mavenclad (cladribine) or Lemtrada (alemtuzumab) which broadly suppress lymphocytes.
What it does: Produces IFN-γ which activates macrophages to attack myelin. Classic pathway identified in early MS research.
Key markers we test: IFN-γ, IL-12, TNF-α
Clinical significance: Often seen with Th17 activation. Tysabri (natalizumab) blocks migration of these cells into the CNS.
Neurofilament Light Chain (NFL): Gold standard marker of ongoing nerve damage—shows if your current treatment is working
GFAP: Marker of astrocyte activation and neurodegeneration
MMP-9: Breaks down blood-brain barrier allowing immune cells in
JC Virus Antibodies: Critical for assessing PML risk with Tysabri or other high-risk DMTs
MOG/AQP4 Antibodies: Rules out MOG-AD or NMOSD which require different treatments
Understanding if you have active immune attack or burned-out disease
Why this matters: Standard Anti-TPO and Anti-TG tests tell you that you have Hashimoto's—but they don't tell you if the immune attack is still ACTIVE or if it's burned out. IgG subtyping changes everything.
IgG1 & IgG3 (Active Inflammation): These antibody types cause active immune attack and tissue destruction. If these are elevated, your immune system is CURRENTLY attacking your thyroid—immune modulation may help.
IgG4 (Chronic/Burned-Out): This antibody type indicates chronic, less inflammatory disease. If IgG4 dominates, your immune attack has subsided—aggressive immune suppression won't help much.
What it does: T-cells directly attack thyroid tissue, triggering inflammation and gland destruction.
Key markers we test: IFN-γ, IL-2, TNF-α
Clinical significance: High Th1 activity suggests active cellular destruction—may respond to immune modulation with LDN, selenium, or vitamin D.
What it does: IL-17 promotes tissue inflammation and recruits neutrophils to the thyroid gland.
Key markers we test: IL-17A, IL-23, IL-6
Clinical significance: Elevated in more aggressive, inflammatory Hashimoto's. May respond to anti-inflammatory interventions.
Complete Thyroid Panel: TSH, Free T4, Free T3, Reverse T3, TBG—shows if you're converting T4 to active T3
Nutrient Deficiencies: Vitamin D, selenium, zinc, iron—all affect thyroid function and immune regulation
IL-10: Anti-inflammatory cytokine; low levels worsen autoimmune attack
TGF-β: Regulatory cytokine that modulates immune response
This isn't new science—it's established immunology that just hasn't been applied to autoimmune patient care yet.
Oncologists don't say "let's try this chemotherapy and see if it works." They test the tumor's genetics first, then match patients to treatments that target THOSE specific mutations. PathwayBio brings the same precision medicine approach to autoimmune diseases.
The pathways we test have been validated in thousands of research studies. We know that IL-23 inhibitors work for IL-23-dominant patients, B-cell depletion works for B-cell-driven MS, and IgG subtyping predicts Hashimoto's activity. This isn't experimental—it's applying known science to your individual case.
Current practice is trial-and-error because doctors don't have the data. PathwayBio gives you and your doctor the information needed to make an informed decision from the start. It's not a guarantee—but it's a lot better than guessing.
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