Introduction Type 2 immunity (T2), described by high IgE/eosinophils (hIgEe) and allergy, is not an expected primary immunodeficiencies (PI) phenotype outside of syndromes of Hyper IgE, Wiskott, Atypical DiGeorge or Omenn. We uncovered T2 allergic disease novel to four different PIs affecting phagocytes; B cells; thymus/T-cells. Case Description 3-year-old male with persistent bloody diarrhea/nausea/vomit/inflammatory dermatitis, treated for mycobacterial disease due to absent oxidative burst confirmed as X-linked Chronic Granulomatous Disease, found to have hIgEe, cow's milk enterocolitis and IgE-egg allergy. Gut/skin inflammation resolved after cow's milk/egg restrictions. 6-year-old CHARGE syndrome male with lymphopenia/orofacial/midline malformations had acute airway angioedema/tracheitis, revealed as IgE-fire ant (FA) anaphylaxis. Epinephrine was life saving; FA immunotherapy planned. 9-year-old female with nasal hypertrophy, speech delay, upper respiratory infections (URIs) without cardiac defect had allergic-cat rhinoconjunctivitis, confirmed as IgE-cat/dog and 22q11 deletion/T-cell lymphopenia; DiGeorge Syndrome-allergy care followed. 4-year-old male with allergic rhinitis/asthma/hIgEe of unsuspecting PI due to normal immunoglobulins with allergic airways; for URIs, B cells measured, resulted low, then brutons tyrosine kinase mutation confirmed. On IgG replacement, but allergic symptoms persist. Discussion Our experience illustrates risk for delay/masquerade and co-existence of allergy: PI. T2 is recently described to include innate lymphoid cells (ILCs) that belong to lymphoid lineage, are innate yet not myeloid/dendritic. ILCs’ are inflammatory, homeostatic and protective, analogous to T and NK cells, but when dysregulated result in allergic disease. Allergy in PIs may be emerging with increasing prevalence of atopy, may occur with any PI and ILCs are a plausible explanation that warrants further study. Type 2 immunity (T2), described by high IgE/eosinophils (hIgEe) and allergy, is not an expected primary immunodeficiencies (PI) phenotype outside of syndromes of Hyper IgE, Wiskott, Atypical DiGeorge or Omenn. We uncovered T2 allergic disease novel to four different PIs affecting phagocytes; B cells; thymus/T-cells. 3-year-old male with persistent bloody diarrhea/nausea/vomit/inflammatory dermatitis, treated for mycobacterial disease due to absent oxidative burst confirmed as X-linked Chronic Granulomatous Disease, found to have hIgEe, cow's milk enterocolitis and IgE-egg allergy. Gut/skin inflammation resolved after cow's milk/egg restrictions. 6-year-old CHARGE syndrome male with lymphopenia/orofacial/midline malformations had acute airway angioedema/tracheitis, revealed as IgE-fire ant (FA) anaphylaxis. Epinephrine was life saving; FA immunotherapy planned. 9-year-old female with nasal hypertrophy, speech delay, upper respiratory infections (URIs) without cardiac defect had allergic-cat rhinoconjunctivitis, confirmed as IgE-cat/dog and 22q11 deletion/T-cell lymphopenia; DiGeorge Syndrome-allergy care followed. 4-year-old male with allergic rhinitis/asthma/hIgEe of unsuspecting PI due to normal immunoglobulins with allergic airways; for URIs, B cells measured, resulted low, then brutons tyrosine kinase mutation confirmed. On IgG replacement, but allergic symptoms persist. Our experience illustrates risk for delay/masquerade and co-existence of allergy: PI. T2 is recently described to include innate lymphoid cells (ILCs) that belong to lymphoid lineage, are innate yet not myeloid/dendritic. ILCs’ are inflammatory, homeostatic and protective, analogous to T and NK cells, but when dysregulated result in allergic disease. Allergy in PIs may be emerging with increasing prevalence of atopy, may occur with any PI and ILCs are a plausible explanation that warrants further study.