Author/Editor		Porenta-Bešić, Vlasta; Kuhar, Marijana
Title		Kronični potek alergijskih bolezni
Translated title		Chronicity of the allergic disease
Type		članek
Source		Med Razgl
Vol. and No.		Letnik 38, št. Suppl 7
Publication year		1999
Volume		str. 131-7
Language		slo
Abstract		Chronic type of allergic tissue reactions is a combination of type I and type IV a2 hypersensitivity responses. Antigen induces release of performed (the principle mediator is histamine) and newly formed mediators by mast cells. These reactions occur within minutes and have a prolonged effect within several hours. Mastocyts may also contribute to chronic allergic reactions by releasing cytokins. Antigen is presented to Th2 type helper lymphocytes by antigen presenting cells. Th2 cells release interleukin-4, which is an essential cofactor for IgE synthesis by B cells. Th2 cells also release other mediators which are referred to as eosinophil-activating cytokines. Eosinophils themselves synthetise, store and secrete several cytokines. They are influenced by cell adhesion molecules. Eosinophil recruitment may result from local release of chemokines and cytokines. Activated eosinophils are believed to cause allergic tissue damage through the release of basic proteins from the crystalloid granule as well as from membrane-derived lipids such as leukotriens.
Summary		Kronični tip alergijske reakcije je kombinacija med tipom I in IV a2 preobčutljivostnega odgovora. Antigen stimulira mastocit k sprožanju že obstoječih (glavni je histamin) in na novo oblikovanih posrednikov vnetja. Ta reakcija se začne v nekaj minutah in traja več ur. Mastociti pa sproščajo tudi nekatere citokine, zaradi katerih je antigen udeležen tudi v kroničnem vnetnem dogajanju. Preko antigen predstavitvenih celic je tudi predstavljen limfocit Th2, ki izloča interlevkin-4, ta pa je pomemben sprožilec tvorbe IgE v limfocitu B. Th2 limfocit pa sprošča tudi druge mediatorje, ki vključijo eozinofilce v vnetni proces. Tudi eozinofilci tvorijo, skladiščijo in sproščajo številne citokine. Nanje vplivajo adhezijske molekule, na njihovo aktivacijo in pojavljanje na mestu vnetja pa vplivajo kemokini in citokini, ki nastajajo lokalno. Aktivirani eozinofilci sproščajo bazični protein iz kristaloidnih granul in levkotriene ter druge mediatorje iz membranskih lipidov, ki povzročajo poškodbo tkiva na mestu vnetja.
Descriptors		HYPERSENSITIVITY, IMMEDIATE HYPERSENSITIVITY, DELAYED MAST CELLS EOSINOPHILS CHEMOTAXIS, LEUKOCYTE GLUCOCORTICOIDS