Doğuş Altunöz
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Doğuş Altunöz has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Barbara Ursula Schraml
Institute for Immunology, Biomedical Center, LMU Medizin, LMU Munich, Planegg-Martinsried, Germany
2 shared publications - Ramin Shakiba
Biomedical Center, Institute of Cardiovascular Physiology and Pathophysiology
2 shared publications - Ayca Sayi-Yazgan
Department of Molecular Biology and Genetics, Faculty of Science and Letters, Istanbul Technical University, Istanbul, Turkey
1 shared publication - Nikos E. Papaioannou
Biomedical Research Foundation of the Academy of Athens, Athens, Greece
1 shared publication
Latest Publications
- 29 March 2025
- Published by EMBL-EBI
scRNAseq of dendritic cells and CD90+ cells from the spleens of 3-week-old Clec9a-cre Stat1-flox/flox mice and Stat1-flox/flox control mice.
BioStudies – one package for all the data supporting a study
- 29 March 2025
- Published by EMBL-EBI
scRNAseq of dendritic cells and CD90+ cells from the spleens of 3-week-old Clec9a-cre Stat1-flox/flox mice and Stat1-flox/flox control mice.
BioStudies – one package for all the data supporting a study
- 26 March 2025
- Published by EMBL-EBI
scRNAseq of splenic dendritic cells across age
BioStudies – one package for all the data supporting a study
- 26 March 2025
- Published by EMBL-EBI
scRNAseq of splenic dendritic cells across age
BioStudies – one package for all the data supporting a study
- Open Access
- 20 April 2021
- Published by The Scientific and Technological Research Council of Turkey (TUBITAK-ULAKBIM) - DIGITAL COMMONS JOURNALS in TURKISH JOURNAL OF BIOLOGY
- Vol. 45 (2) , 214-224
Helicobacter-stimulated IL-10-producing B cells suppress differentiation of lipopolysaccharide/Helicobacter felis-activated stimulatory dendritic cells
Regulatory B cells (Bregs) produce antiinflammatory cytokines and inhibits proinflammatory response. Recently, immunosuppressive roles of Bregs in the effector functions of dendritic cells (DCs) were demonstrated. However, cross talk between Bregs and DCs in Helicobacter infection remains unknown. Here, we showed that direct stimulation of bone marrow-derived DCs (BM-DCs) with Helicobacter felis (H. felis) antigen upregulates their CD86 surface expression and causes the production of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interleukin-12 (IL-12), and interleukin-10 (IL-10). Furthermore, prestimulation of DCs with supernatants derived from both Helicobacter-stimulated IL-10- B (Hf stim-IL-10- B) or IL-10+ B (Hf stim-IL-10+) cells suppresses the secretion of TNF-alpha and IL-6, but does not affect the expression of CD86 and secretion of IL-12 by lipopolysaccharide (LPS) or H. felisactivated BM-DCs. Remarkably, soluble factors secreted by Hf stim-IL-10- B cells, but not by Hf stim-IL-10+ B cells, suppress the secretion of IL-10 by BM-DCs upon subsequent LPS stimulation. In contrast, prestimulation with BM-DCs with supernatants of Hf stim-IL-10+ B cells before H. felis antigen stimulation induces significantly their IL-10 production. Collectively, our data indicated that prestimulation with soluble factors secreted by Hf stim-IL-10+ B cells, DCs exhibit a tolerogenic phenotype in response to LPS or Helicobacter antigen by secreting high levels of IL-10, but decreased levels of IL-6 and TNF-alpha.
- 20 April 2021
- Published by The Scientific and Technological Research Council of Turkey (TUBITAK-ULAKBIM) - DIGITAL COMMONS JOURNALS in TURKISH JOURNAL OF BIOLOGY
- Vol. 45 (2) , 214-224
Open AccessHelicobacter-stimulated IL-10-producing B cells suppress differentiation of lipopolysaccharide/Helicobacter felis-activated stimulatory dendritic cells
Regulatory B cells (Bregs) produce antiinflammatory cytokines and inhibits proinflammatory response. Recently, immunosuppressive roles of Bregs in the effector functions of dendritic cells (DCs) were demonstrated. However, cross talk between Bregs and DCs in Helicobacter infection remains unknown. Here, we showed that direct stimulation of bone marrow-derived DCs (BM-DCs) with Helicobacter felis (H. felis) antigen upregulates their CD86 surface expression and causes the production of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interleukin-12 (IL-12), and interleukin-10 (IL-10). Furthermore, prestimulation of DCs with supernatants derived from both Helicobacter-stimulated IL-10- B (Hf stim-IL-10- B) or IL-10+ B (Hf stim-IL-10+) cells suppresses the secretion of TNF-alpha and IL-6, but does not affect the expression of CD86 and secretion of IL-12 by lipopolysaccharide (LPS) or H. felisactivated BM-DCs. Remarkably, soluble factors secreted by Hf stim-IL-10- B cells, but not by Hf stim-IL-10+ B cells, suppress the secretion of IL-10 by BM-DCs upon subsequent LPS stimulation. In contrast, prestimulation with BM-DCs with supernatants of Hf stim-IL-10+ B cells before H. felis antigen stimulation induces significantly their IL-10 production. Collectively, our data indicated that prestimulation with soluble factors secreted by Hf stim-IL-10+ B cells, DCs exhibit a tolerogenic phenotype in response to LPS or Helicobacter antigen by secreting high levels of IL-10, but decreased levels of IL-6 and TNF-alpha.