Inflammation Categorization
This cytokine causes B-cell class switching to IgE.
What is IL-4?
This biologic binds IgE.
What is omalizumab?
This therapy must already be maximized before biologics.
What is high-dose ICS + LABA?
This biomarker reflects nitric oxide inflammation.
What is FeNO?
A patient with eosinophilic asthma needs this class.
What are IL-5 inhibitors?
These epithelial mediators initiate Type 2 inflammation.
What are alarmins (TSLP, IL-33, IL-25)?
This biologic blocks IL-4 and IL-13.
What is dupilumab?
This number of exacerbations supports severe asthma.
What is ≥2 exacerbations/year?
This FeNO level suggests Type 2 inflammation.
What is >25 ppb?
A patient who prefers infrequent dosing may benefit from this drug.
What is depemokimab?
This T-helper subtype drives allergic asthma inflammation.
What is Th2?
This biologic works upstream and is independent of biomarkers.
What is tezepelumab?
This phenotype qualifies for omalizumab.
What is allergic asthma?
This biologic does NOT require biomarker elevation.
What is tezepelumab?
A patient who wants IV therapy receives this biologic.
What is reslizumab?
These innate immune cells can produce IL-5 and IL-13 without T-cell activation.
What are ILC2 cells?
This biologic causes eosinophil apoptosis via IL-5 receptor binding.
What is benralizumab?
This phenotype qualifies for IL-5 biologics.
What is eosinophilic asthma?
This drug excludes patients with eosinophils >1500.
What is dupilumab?
Severe asthma + high IgE + allergic triggers → best biologic.
What is omalizumab?
This combination of effects defines Type 2 asthma pathology.
What is IgE-mediated hypersensitivity + eosinophilic inflammation?
This biologic has the longest dosing interval (every 6 months).
What is depemokimab?
This condition must be ruled out before escalating therapy.
What is poor adherence or incorrect inhaler use?
This biomarker is NOT routinely used clinically despite relevance.
What is periostin?