Emre D. Cardakli

ORCID: 0000-0002-8473-0558
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About
Contact & Profiles
Research Areas
  • interferon and immune responses
  • Galectins and Cancer Biology
  • Mycobacterium research and diagnosis
  • Immune responses and vaccinations
  • Immune cells in cancer
  • Eosinophilic Esophagitis
  • Inflammatory Bowel Disease
  • Cancer-related molecular mechanisms research
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Cytokine Signaling Pathways and Interactions
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immune Response and Inflammation
  • Infant Nutrition and Health

Duke University
2020-2022

Cornell University
2022

Weill Cornell Medicine
2022

Tri-Institutional PhD Program in Chemical Biology
2022

Rockefeller University
2022

Memorial Sloan Kettering Cancer Center
2022

Endoplasmic reticulum (ER) stress is associated with Crohn's disease (CD), but its impact on host-microbe interaction in pathogenesis not well defined. Functional deficiency the protein disulfide isomerase anterior gradient 2 (AGR2) has been linked CD and leads to epithelial cell ER ileocolitis mice humans. Here, we show that ileal expression of AGR2 correlates mucosal Enterobactericeae abundance human inflammatory bowel (IBD) Agr2 deletion ER-stress-dependent expansion mucosal-associated...

10.1016/j.celrep.2022.111637 article EN cc-by Cell Reports 2022-11-01

Abstract Dectin-1 is known to drive proinflammatory cytokine production by macrophages and dendritic cells which promotes Th17 CD4+ T cell responses in the setting of fungal infection. However, role signaling neutrophils its impact on not well understood. In this study, we found that stimulated with a agonist diminish viability rapid reactive oxygen species (ROS)-dependent manner. Furthermore, promoted neutrophil PD-L1 expression via Syk Card9 signaling, along other immune-checkpoint factors...

10.1002/jlb.3a0322-152rr article EN Journal of Leukocyte Biology 2022-09-08

ABSTRACT Pathologic roles for innate immunity in neurologic disorders are well-described, but protective aspects of the immune response less understood. Dectin-1, a C-type lectin receptor (CLR), is largely known to induce inflammation. However, we found that Dectin-1 experimental autoimmune encephalomyelitis (EAE), while its canonical signaling mediator, Card9, promotes disease. Notably, does not respond heat-killed Mycobacteria , an adjuvant EAE. Myeloid cells mediate function EAE and...

10.1101/2020.05.06.080481 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-05-08

Abstract Innate immunity mediates both damage and repair of the central nervous system (CNS) in neurologic disorders. Although pathologic roles for innate are well-described multiple sclerosis (MS) its animal model, experimental autoimmune encephalomyelitis (EAE), protective aspects immune response less understood. In this study, we sought to identify function Dectin-1, a C-type lectin receptor (CLR), CNS autoimmunity. We found that Dectin-1 limited neuroinflammation EAE while canonical...

10.4049/jimmunol.206.supp.96.07 article EN The Journal of Immunology 2021-05-01
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