[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.204.95.166. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Article
October 1981

Immunopathology of Ascarid Infection of the EyeRole of IgE Antibodies and Mast Cells

Author Affiliations

From the Department of Ophthalmology, Scheie Eye Institute, School of Medicine (Drs Rockey, Donnelly, and Laties), and the Department of Pathobiology, School of Veterinary Medicine (Drs Stromberg and Soulsby), University of Pennsylvania, Philadelphia. Dr Stromberg is now at the University of Minnesota, St Paul. Dr Soulsby is now at the University of Cambridge (England).

Arch Ophthalmol. 1981;99(10):1831-1840. doi:10.1001/archopht.1981.03930020705017
Abstract

• The roles of IgE antiascarid antibodies and mast cells were compared in passively sensitized guinea pigs and animals infected intravitreally with ascarid larvae (Toxocara canis, Ascaris suum). Intravenous IgE antibody disappeared from the serum within 48 hours, but induced a hypersensitive state that persisted for 28 days. In systemically immunized animals, the aqueous-serum IgE antibody ratio was 1:1,000 or less. Passive periocular anaphylactic reactions produced an infiltration of neutrophils and eosinophils, degranulation of mast cells, and vascular leakage in periocular and episcleral tissues. Systemic anaphylaxis also produced degranulation of uveal mast cells, an infiltration of eosinophils, and vascular leakage in the choroid. Intraocular infection produced a transient decrease of mast cells that correlated with an increased infiltration of eosinophils and plasma cells.

×