Degranulation in mast cells is part of an inflammatory response, and substances such as histamine are released. Granules from mast cells mediate processes such as "vasodilation, vascular homeostasis, innate and adaptive immune responses, angiogenesis, and venom detoxification."[1]
Antigens interact withIgE molecules already bound to high affinityFc receptors on the surface ofmast cells to induce degranulation, via the activation of tyrosine kinases within the cell. The mast cell releases a mixture of compounds, includinghistamine,proteoglycans,serotonin, andserine proteases from its cytoplasmic granules.[2]
In a similar mechanism, activated eosinophils release preformed mediators such asmajor basic protein, andenzymes such asperoxidase, following interaction between their Fc receptors and IgE molecules that are bound to largeparasites likehelminths.[3][4]
Degranulation in neutrophils can occur in response to infection, and the resulting granules are released in order to protect against tissue damage. Excessive degranulation of neutrophils, sometimes triggered by bacteria, is associated with certain inflammatory disorders, such as asthma and septic shock.[5][6]
Four kinds of granules exist in neutrophils that display differences in content and regulation. Secretory vesicles are the most likely to release their contents by degranulation, followed bygelatinase granules,specific granules, andazurophil granules.[7][8]
^Yamasaki S, Saito T (2005). "Regulation of mast cell activation through FcepsilonRI".Chem Immunol Allergy. Chemical Immunology and Allergy.87:22–31.doi:10.1159/000087568.ISBN3-8055-7948-9.PMID16107760.
^David J, Butterworth A, Vadas M (1980). "Mechanism of the interaction mediating killing of Schistosoma mansoni by human eosinophils".Am J Trop Med Hyg.29 (5):842–8.doi:10.4269/ajtmh.1980.29.842.PMID7435788.
