Author/Editor		Orel, R
Title		Nekatere novosti na področju imunologije celiakije
Translated title		Some new aspects on the immunology of celiac disease
Type		članek
Source		Slov Pediatr
Vol. and No.		Letnik 7, št. Suppl 1
Publication year		2000
Volume		str. 75-8
Language		slo
Abstract		Celiac disease is characterised by a pathologic immune response to dietary gluten-derived antigens in genetically susceptible individuals, carrying characteristics of both food hypersensitivity and autoimmune disease. The effector phase of this abnormal immune response is rather well known. The T-cell mediated, and to a lesser degree the humoral immune mechanisms, take part in damaging the small bowel mucosa and in creating a clinical picture of celiac disease. Normal immune response to ingested food antigens is tolerance but in celiac patients an active immune response is generated against the gluten-derived antigens. Active immunity instead of immune tolerance is induced by the predominant T-helper Th1 type instead of the Th2 /Th3 type of response. A possible reason for this type of response are disturbances in the induction phase of immune response at the time of first contact of gluten-derived antigens with the gut immune system. The induction of a specific type of immune response could happen in a certain state of activation of the gut immune system caused by an infection, direct gluten toxicity, molecular mimicry between gluten and bacterial or viral superantigens, etc. Molecules of gliadin could act as lectines and bond to some of the HLA-molecules - this would explain the genetic predisposition linked to certain HLA genes. Celiac disease shares many characteristics of autoimmune diseases. One of them are the specific tissue antibodies such as endomysial, reticulin and jejunal antibodies. It seems that tissue transglutaminase (tTG) is one of the crucial antigens responsible for their formation. This enzyme is probably involved in the gliadin metabolism. Its action on gliadin molecules may expose new epitopes, responsible for the T lymphocyte activation. Gliadin-tTG complexes may act as a hapten-carrier and costimulate both T and B-lymphocytes to produce autoantibodies.
Summary		Celiakija je posledica nenormalnega imunskega odziva na antigene iz glutena pri osebah z genetsko pogojenim nagnjenjem. Ima tako značilnosti preobčutljivostne reakcije na prehranske alergene (alergije) kot avtoimune bolezni. Efektorski del nenormalnega imunskega odziva pri bolnikih s celiakijo je dokaj dobro znan. Vključuje mehanizme celičnega imunskega odziva in v manjši meri humoralnega, ki vodijo v nastanek sprememb v črevesni sluznici in simptomatsko bolezen. Normalen odziv črevesnega imunskega sistema na prehranske antigene je razvoj tolerance. Pri bolnikih s celiakijo pa se na antigene iz glutena razvije aktivna imunost. Prevladajo aktivnosti celic T pomagalk tipa Th1 nad tipom Th2/Th3. Možni vzrok so motnje, nastale v fazi indukcije imunskega odziva ob prvem srečanju črevesnega imunskega sistema z glutenom. Ta bi lahko potekala v posebnem vzburjenem stanju imunskega sistema npr. zaradi okužbe, direktne toksičnosti glutena, podobnosti med glutenskimi antigeni in mikrobnimi superantigeni; lahko pa bi se gliadinske molekule kot lektini vezali na nekatere molekule HLA, kar bi pojasnilo genetsko nagnjenost pri osebah z določenimi geni HLA. Celiakija ima številne značilnosti avtoimunih bolezni. Značilen je pojav specifičnih tkivnih protiteles, kot so endomizijska, retikulinska in jejunalna. Kaže, da je eden ključnih antigenov za njihovo tvorbo tkivna transglutaminaza (tTG), encim, ki je verjetno vpleten tudi v presnovo gliadina. Z encimskim delovanjem tTG se na gliadinskih molekulah razgalijo novi epitopi, kar lahko spodbudi T-limfocitni odziv. Kompleksi med gliadinom in tTG pa lahko kot hapten-nosilec ob hkratni stimulaciji limfocitov T sprožijo B-limfocitni odziv s tvorbo avtoprotiteles.
Descriptors		CELIAC DISEASE CHILD