Természetes ölő (NK) T lymphocyták légúti gyulladásokban = Natural killer (NK) T lymphocytes in airway inflammation

1.A termeszetes olősejtek altal keltett leguti gyulladas szteroid gyulladasgatloval szemben rezisztens. 2.Ebben a modellben csokken az allergiaval szembeni tolerancia es fokozodik egy viszonylag ujabban felfedezett gyulladaskeltő mediator, az interleukin-17 (IL-17) szintezise a tudőben. 3. Az IL-17 hianya a fenti modellben szteroid rezisztensse teszi a leguti hyperreaktivitast. 4. Szteroid rezisztens leguti allergia (asthma) modellunkben microarray technikaval talaltunk mintegy 23 olyan gent, melyeknek a szteroid rezisztencia kialakulasaban szerepe lehet. 5. Terhes asthmas betegekben igazoltuk, hogy a Treg sejtek szambeli fokozodasa elmarad, mely egeszseges terhessegben egyebkent jellemző. Az anyai asthma tehat csokkenti a terhesseg alatti immuntoleranciat. 6. Ugyanerre utalt a szerum HSP70 koncentracio, valamint a Th17/Treg sejtarany emelkedese is asthmas terhesekben. 7. Egeszseges terhesekben osszefugg a Treg sejtek szamanak fokozodasa (immuntolerancia) a magzati novekedes fiziologias mertekevel. Asthmas terhesekben a Treg szam nem nő es nincs osszefugges a Treg szam es a magzati szuletesi suly kozott. 8.Szamos eredmeny szuletett a dohanyzas altal kivaltott kiserletes pulmonalis hypertonia pathomechanizmusarol, a cisplatinnal kapcsolatos nephropathia kockazati telnyezőiről, valamint az asthma es a tudőrak kulonfele biomarkereiről. | 1.Airway inflammation induced by the activation of natural killers proved to be resistant to treatment by steroid antiinflammatory agents. 2.In this model, tolerance against the development of allergies is decreased and the synthesis of interleukin-17 (IL-17), a recently discovered proinflammatory mediator, is increased. 3.Absence of IL-17 in this model of asthma makes airway inflammation steroid resistant. 4.In our earlier, steroid resistant airway allergy model, using microarray technique, we have identified 23 genes possibly responsible for steroid resistance. 5.The increase of Treg cells in healthy pregnancy is absent in pregnant patients suffering from asthma. Thus, asthma interferes with natural immunotolerance of pregnancy. 6.The same conclusion can be drawn basen on the increase of heat-shock protein-70 and the Th17/Treg ratio in asthmatic pregnants. 7.There is a relationship between the abundance of maternal Tregs and the birth weight of newborns in healthy pregnants. This relationship is absent in asthmatic pregnants as is the abundance of Tregs. 8. Many new findings have been published by us about the mechanism of experimental pulmonary hypertension induced by smoking and nephropathy induced by cisplatin (in lung cancer patients). New biomarkers (in the exhaled breath) were identified in asthmatics and lung cancer patients.