Esen Yonca Bassoy

Dr. Esen Yonca Bassoy

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Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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16 December 2017 in Immunological Reviews
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Journal Article
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Esen Yonca BassoyEsen Yonca Bassoy
Esen Yonca Bassoy
JTJennifer E Towne
Jennifer E Towne
CGCem Gabay
Cem Gabay

31 October 2014 in Cell Death & Differentiation
Verified
Journal Article
Closed access
GJG Jacquemin
G Jacquemin
DMD Margiotta
D Margiotta
AKA Kasahara
A Kasahara
Esen Yonca BassoyEsen Yonca Bassoy
Esen Yonca Bassoy
MWM Walch
M Walch
DMD Martinvalet
D Martinvalet

24 November 2017 in Nature Communications
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Journal Article
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PNPaula Nunes-Hasler
Paula Nunes-Hasler
SMSophia Maschalidi
Sophia Maschalidi
CLCarla Lippens
Carla Lippens
CCCyril Castelbou
Cyril Castelbou
SBSamuel Bouvet
Samuel Bouvet
NDNicolas Demaurex
Nicolas Demaurex
Antigen cross-presentation by dendritic cells (DC) stimulates cytotoxic T cell activation to promote immunity to intracellular pathogens, viruses and cancer. Phagocytosed antigens generate potent T cell responses, but the signalling and trafficking pathways regulating their cross-presentation are unclear. Here, we show that ablation of the store-operated-Ca2+-entry regulator STIM1 in mouse myeloid cells impairs cross-presentation and DC migration in vivo and in vitro.Stim1ablation reduces Ca2+signals, cross-presentation, and chemotaxis in mouse bone-marrow-derived DCs without altering cell differentiation, maturation or phagocytic capacity. Phagosomal pH homoeostasis and ROS production are unaffected by STIM1 deficiency, but phagosomal proteolysis and leucyl aminopeptidase activity, IRAP recruitment, as well as fusion of phagosomes with endosomes and lysosomes are all impaired. These data suggest that STIM1-dependent Ca2+signalling promotes the delivery of endolysosomal enzymes to phagosomes to enable efficient cross-presentation.

28 April 2020 in Life Science Alliance
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JGJérémie D Goldstein
Jérémie D Goldstein
Esen Yonca BassoyEsen Yonca Bassoy
Esen Yonca Bassoy
ACAssunta Caruso
Assunta Caruso
JPJennifer Palomo
Jennifer Palomo
EREmiliana Rodriguez
Emiliana Rodriguez
CGCem Gabay
Cem Gabay
IL-36R signaling plays an important role in the pathogenesis of psoriasis. We ought to assess the specific function of IL-36R in keratinocytes for the pathology of Aldara-induced psoriasis-like dermatitis. Il36rΔK mice presenting deletion of IL-36R in keratinocytes were similarly resistant to Aldara-induced ear inflammation as Il36r−/− mice, but acanthosis was only prevented in Il36r−/− mice. FACS analysis revealed that IL-36R signaling in keratinocytes is mandatory for early neutrophil infiltration in Aldara-treated ears. RNASeq and qRT-PCR experiments demonstrated the crucial role of IL-36R signaling in keratinocytes for induction of IL-23, IL-17, and IL-22 at early time points. Taken together, our results demonstrate that IL-36R signaling in keratinocytes plays a major role in the induction of Aldara-induced psoriasis-like dermatitis by triggering early production of IL-23/IL-17/IL-22 cytokines and neutrophil infiltration.

24 March 2017 in Cell Death & Differentiation
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Journal Article
Closed access
VCValentina Chiusolo
Valentina Chiusolo
GJGuillaume Jacquemin
Guillaume Jacquemin
Esen Yonca BassoyEsen Yonca Bassoy
Esen Yonca Bassoy
LVLaurent Vinet
Laurent Vinet
LLLavinia Liguori
Lavinia Liguori
DMDenis Martinvalet
Denis Martinvalet

10 March 2017 in The EMBO Journal
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Journal Article
Closed access
PDF file
Esen Yonca BassoyEsen Yonca Bassoy
Esen Yonca Bassoy
AKAtsuko Kasahara
Atsuko Kasahara
VCValentina Chiusolo
Valentina Chiusolo
GJGuillaume Jacquemin
Guillaume Jacquemin
EBEmma Boydell
Emma Boydell
DMDenis Martinvalet
Denis Martinvalet