| − | Unlike [[IgM]], [[IgG]] and [[IgA]], IgE does not function as a soluble antibody, with binding to Fcε receptors before it can bind to the target, and is found in low levels in blood plasma. Like [[IgA]], it is produced by plasma cells and is mainly localised to mucosal surfaces. | + | Unlike [[IgM]], [[IgG]] and [[IgA]], IgE does not function as a soluble antibody, with binding to Fcε receptors required before it can bind to the target antigen, and is found in low levels in blood plasma. Like [[IgA]], it is produced by [[B cell differentiation|plasma cells]] and is mainly localised to mucosal surfaces. |
| − | IgE triggers acute inflammation by binding to the FCεRI receptors on mast cells in the lamina propria and [[Basophils|basophils]], causing degranulation. It is involved in [[Type I Hypersensitivity|type I hypersensitivity reactions]]. Cross-linking of IgE molecules by antigens, triggers [[Mast Cells|mast cell]] degranulation and an inflammatory response. IgE has considerable involvement in producing immunity to parasitic worms, particularly [[:Category:Nematodes|nematode]] parasites. It may mediate their expulsion or killing via mast cell activity, cytotoxic [[Eosinophils|eosinophils]], [[Macrophages|macrophages]], and so on. | + | IgE triggers acute inflammation by binding to the FCεRI receptors on mast cells in the lamina propria and [[Basophils|basophils]], causing degranulation when bound to target. It is involved in [[Type I Hypersensitivity|type I hypersensitivity reactions]]. Cross-linking of IgE molecules by antigens, triggers [[Mast Cells|mast cell]] and [[Eosinophil|eosinophil]] degranulation and an inflammatory response. IgE has considerable involvement in producing [[Immunity to Parasites|immunity to parasitic worms]], particularly [[:Category:Nematodes|nematode]] parasites. It may mediate their expulsion or killing via mast cell activity, cytotoxic [[Eosinophils|eosinophils]], [[Macrophages|macrophages]], and so on. |