Yazar "Artac H." seçeneğine göre listele
Listeleniyor 1 - 2 / 2
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe The clinical value of interleukins-8, -10, and -17 in idiopathic granulomatous mastitis(Springer, 2020) Koksal H.; Vatansev H.; Artac H.; Kadoglou N.Introduction: Idiopathic granulomatous mastitis (IGM) is a rare, chronic inflammatory benign breast disease. Although the etiology of this disease is unknown, it has been suggested that hormonal disorders, autoimmunity, smoking, and ?1-antitrypsin deficiency may play a role in the etiopathogenesis. The aim is to investigate the changes in cytokine profiles including interleukin (IL)-4, -8, -10, -17, and tumor necrosis factor (TNF)-alpha in patients with IGM. Methods: Forty-seven patients with pathologically diagnosed IGM and 30 healthy women were included. The cytokines including IL-4, -8, 10, -17, and TNF-alpha were measured by human enzyme-linked immunosorbent assay. Results: The IL-8, IL-10, and IL-17 levels were higher in IGM patients than control group (p =.002; p =.008; and p =.018, respectively). The IL-8 levels of patients with active lesions and in remission were statistically higher than the control group (p =.027 and p =.015, respectively). IL-10 levels of patients in remission were higher than the control group (p =.024). There was no difference in IL-4 and TNF-? levels between all groups. Conclusion: These results showed that proinflammatory cytokines including IL-8 and IL-17 have role in pathogenesis of IGM. However, the increased levels of IL-10 in especially patients in remission suggest that it reduces the release of proinflamatory cytokines as well as suppressing their function and activation for controlling IGM. Although IGM is thought to be a surgical disease, these cytokine changes indicate the presence of serious immune dysregulation. This suggests that in the treatment of IGM, treatment needs to evolve from surgery to medical treatment.Key points The IL-8, IL-10, and IL-17 levels were higher in IGM patients than in control group. The IL-8 levels of both patients with active lesions and in remission were high. There was no difference in IL-4 and TNF-? levels between all groups. © 2020, International League of Associations for Rheumatology (ILAR).Öğe ILC3 deficiency and generalized ILC abnormalities in DOCK8-deficient patients(Blackwell Publishing Ltd, 2019) Eken A.; Cansever M.; Okus F.Z.; Erdem S.; Nain E.; Azizoglu Z.B.; Haliloglu Y.; Karakukçu M.; Ozcan A.; Devecioğlu O.; Aksu G.; Ayyildiz Z.A.; Topal E.; Aydiner E.K.; Kiykim A.; Metin A.; Cipe F.; Kaya A.; Artac H.; Reisli I.; Guner S.N.; Uygun V.; Karasu G.; Altuntas H.D.; Canatan H.; Oukka M.; Ozen A.; Chatila T.A.; Keles S.; Baris S.; Unal E.; Patiroglu T.Background: Dedicator of cytokinesis 8 (DOCK8) deficiency is the main cause of the autosomal recessive hyper-IgE syndrome (HIES). We previously reported the selective loss of group 3 innate lymphoid cell (ILC) number and function in a Dock8-deficient mouse model. In this study, we sought to test whether DOCK8 is required for the function and maintenance of ILC subsets in humans. Methods: Peripheral blood ILC1-3 subsets of 16 DOCK8-deficient patients recruited at the pretransplant stage, and seven patients with autosomal dominant (AD) HIES due to STAT3 mutations, were compared with those of healthy controls or post-transplant DOCK8-deficient patients (n = 12) by flow cytometry and real-time qPCR. Sorted total ILCs from DOCK8- or STAT3-mutant patients and healthy controls were assayed for survival, apoptosis, proliferation, and activation by IL-7, IL-23, and IL-12 by cell culture, flow cytometry, and phospho-flow assays. Results: DOCK8-deficient but not STAT3-mutant patients exhibited a profound depletion of ILC3s, and to a lesser extent ILC2s, in their peripheral blood. DOCK8-deficient ILC1-3 subsets had defective proliferation, expressed lower levels of IL-7R, responded less to IL-7, IL-12, or IL-23 cytokines, and were more prone to apoptosis compared with those of healthy controls. Conclusion: DOCK8 regulates human ILC3 expansion and survival, and more globally ILC cytokine signaling and proliferation. DOCK8 deficiency leads to loss of ILC3 from peripheral blood. ILC3 deficiency may contribute to the susceptibility of DOCK8-deficient patients to infections. © 2019 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.