Laboratory animal allergy (LAA) results from occupational ex-posure to allergens found in the hair, dander, urine, and salivaof laboratory animals. It presents as work-related rhinocon-junctivitis and occupational asthma after a latency period of2–3 years. Prevalence of rodent-sensitisation among laboratoryanimal (LA) workers ranges between 10.4% [1] and 28% [2].Though exposure is a major risk factor, some individuals developallergen-specific IgE without progressing to LAA symptoms andare considered clinically tolerant [3]. High levels of LA exposureare linked to allergic tolerance [2, 4, 5] potentially mediated bytolerance-associated molecules such as allergen-specific IgG4,which have been shown to inhibit allergic immune mechanisms[6]. Most LAA studies were conducted before changes in animalhousing from open cages to individually ventilated cages (IVCs);this has resulted in lower exposure levels. We examined asso-ciations between current exposures, sensitisation, and clinicaltolerance in a modern LA workforce
J.Canizales, S.Schofield, M. H.Shamji, P.Cullinan, M.Jones, and J.Feary, “Patterns of Mouse Allergen–Specific IgE and IgG4 in Contemporary Animal Research Environments,” Clinical & Experimental Allergy (2026): 1–3, https://doi.org/10.1111/cea.70307.
