Nicola Laura Diny
@uni-bonn.de
University of Bonn
RESEARCH, TEACHING, or OTHER INTERESTS
Immunology
Scopus Publications
- Editorial: Update on eosinophil-associated diseases
Nicola Laura Diny, Yoshiyuki Yamada, Nives Zimmermann
Frontiers in Allergy, 2025 - Correction: Editorial: Update on eosinophil-associated diseases (Frontiers in Allergy, (2025), 6, (1740057), 10.3389/falgy.2025.1740057)
Nicola Laura Diny, Yoshiyuki Yamada, Nives Zimmermann
Frontiers in Allergy, 2025 - Drosophila AHR limits tumor growth and stem cell proliferation in the intestine
Minghua Tsai, Jiawei Sun, Cyrille Alexandre, Michael Shapiro, Adrien Franchet, et al.
Wellcome Open Research, 2025
Background The aryl hydrocarbon receptor (AHR) plays important roles in intestinal homeostasis, limiting tumour growth and promoting differentiation in the intestinal epithelium. Spineless, the Drosophila homolog of AHR, has only been studied in the context of development but not in the adult intestine. Methods The role of Spineless in the Drosophila midgut was studied by overexpression or inactivation of Spineless in infection and tumour models and RNA sequencing of sorted midgut progenitor cells. Results We show that spineless is upregulated in the adult intestinal epithelium after infection with Pseudomonas entomophila (P.e.). Spineless inactivation increased stem cell proliferation following infection-induced injury. Spineless overexpression limited intestinal stem cell proliferation and reduced survival after infection. In two tumour models, using either Notch RNAi or constitutively active Yorkie, Spineless suppressed tumour growth and doubled the lifespan of tumour-bearing flies. At the transcriptional level it reversed the gene expression changes induced in Yorkie tumours, counteracting cell proliferation and altered metabolism. Conclusions These findings demonstrate a new role for Spineless in the adult Drosophila midgut and highlight the evolutionarily conserved functions of AHR/Spineless in the control of proliferation and differentiation of the intestinal epithelium. - Women in STEM becoming independent: Embrace failures as part of the journey to success
Zhoujie Ding, Nicola Laura Diny, Rebecca Gentek, Shiri Gur-Cohen, Motoko Y. Kimura, et al.
Journal of Experimental Medicine, 2024
This year at JEM, we are highlighting women in science by sharing their stories and amplifying their voices. In this Viewpoint, we hear from a cross section of women, across multiple research fields, discussing their science and the process of setting up a lab as an independent researcher. - The AHR repressor limits expression of antimicrobial genes but not AHR-dependent genes in intestinal eosinophils
Heike Weighardt, Michael Shapiro, Michelle Mayer, Irmgard Förster, Brigitta Stockinger, et al.
Journal of Leukocyte Biology, 2024
Intestinal eosinophils express the aryl hydrocarbon receptor (AHR), an environmental sensor and ligand-activated transcription factor that responds to dietary or environmental ligands. AHR regulates tissue adaptation, survival, adhesion, and immune functions in intestinal eosinophils. The AHR repressor (AHRR) is itself induced by AHR and believed to limit AHR activity in a negative feedback loop. We analyzed gene expression in intestinal eosinophils from wild-type and AHRR knockout mice and found that AHRR did not suppress most AHR-dependent genes. Instead, AHRR limited the expression of a distinct small set of genes involved in the innate immune response. These included S100 proteins, antimicrobial proteins, and alpha-defensins. Using bone marrow–derived eosinophils, we found that AHRR knockout eosinophils released more reactive oxygen species upon stimulation. This work shows that the paradigm of AHRR as a repressor of AHR transcriptional activity does not apply to intestinal eosinophils. Rather, AHRR limits the expression of innate immune response and antimicrobial genes, possibly to maintain an anti-inflammatory phenotype in eosinophils when exposed to microbial signals in the intestinal environment. - Dietary environmental factors shape the immune defense against Cryptosporidium infection
Muralidhara Rao Maradana, N. Bishara Marzook, Oscar E. Diaz, Tapoka Mkandawire, Nicola Laura Diny, et al.
Cell Host and Microbe, 2023 - Hypereosinophilia causes progressive cardiac pathologies in mice
Nicola Laura Diny, Megan Kay Wood, Taejoon Won, Monica Vladut Talor, Clarisse Lukban, et al.
Iscience, 2023 - The aryl hydrocarbon receptor contributes to tissue adaptation of intestinal eosinophils in mice
Nicola Laura Diny, Barbora Schonfeldova, Michael Shapiro, Matthew L. Winder, Sunita Varsani-Brown, et al.
Journal of Experimental Medicine, 2022
Eosinophils are potent sources of inflammatory and toxic mediators, yet they reside in large numbers in the healthy intestine without causing tissue damage. We show here that intestinal eosinophils were specifically adapted to their environment and underwent substantial transcriptomic changes. Intestinal eosinophils upregulated genes relating to the immune response, cell–cell communication, extracellular matrix remodeling, and the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor with broad functions in intestinal homeostasis. Eosinophils from AHR-deficient mice failed to fully express the intestinal gene expression program, including extracellular matrix organization and cell junction pathways. AHR-deficient eosinophils were functionally impaired in the adhesion to and degradation of extracellular matrix, were more prone to degranulation, and had an extended life span. Lack of AHR in eosinophils had wider effects on the intestinal immune system, affecting the T cell compartment in nave and helminth-infected mice. Our study demonstrates that the response to environmental triggers via AHR partially shapes tissue adaptation of eosinophils in the small intestine. - The Cardiac Microenvironment Instructs Divergent Monocyte Fates and Functions in Myocarditis
Xuezhou Hou, Guobao Chen, William Bracamonte-Baran, Hee Sun Choi, Nicola L. Diny, et al.
Cell Reports, 2019 - Sca-1 + cardiac fibroblasts promote development of heart failure
Guobao Chen, William Bracamonte‐Baran, Nicola L. Diny, Xuezhou Hou, Monica V. Talor, et al.
European Journal of Immunology, 2018
The causative effect of GM‐CSF produced by cardiac fibroblasts to development of heart failure has not been shown. We identified the pathological GM‐CSF‐producing cardiac fibroblast subset and the specific deletion of IL‐17A signaling to these cells attenuated cardiac inflammation and heart failure. We describe here the CD45−CD31−CD29+mEF‐SK4+PDGFRα+Sca‐1+periostin+ (Sca‐1+) cardiac fibroblast subset as the main GM‐CSF producer in both experimental autoimmune myocarditis and myocardial infarction mouse models. Specific ablation of IL‐17A signaling to Sca‐1+periostin+ cardiac fibroblasts (PostnCreIl17rafl/fl) protected mice from post‐infarct heart failure and death. Moreover, PostnCreIl17rafl/fl mice had significantly fewer GM‐CSF‐producing Sca‐1+ cardiac fibroblasts and inflammatory Ly6Chi monocytes in the heart. Sca‐1+ cardiac fibroblasts were not only potent GM‐CSF producers, but also exhibited plasticity and switched their cytokine production profiles depending on local microenvironments. Moreover, we also found GM‐CSF‐positive cardiac fibroblasts in cardiac biopsy samples from heart failure patients of myocarditis or ischemic origin. Thus, this is the first identification of a pathological GM‐CSF‐producing cardiac fibroblast subset in human and mice hearts with myocarditis and ischemic cardiomyopathy. Sca‐1+ cardiac fibroblasts direct the type of immune cells infiltrating the heart during cardiac inflammation and drive the development of heart failure. - Whi2 is a conserved negative regulator of TORC1 in response to low amino acids
Xianghui Chen, Guiqin Wang, Yu Zhang, Margaret Dayhoff-Brannigan, Nicola L. Diny, et al.
Plos Genetics, 2018 - Regulation of autoimmune myocarditis by host responses to the microbiome
Jobert G. Barin, Monica V. Talor, Nicola L. Diny, SuFey Ong, Julie A. Schaub, et al.
Experimental and Molecular Pathology, 2017 - Eosinophils in autoimmune diseases
Nicola L. Diny, Noel R. Rose, Daniela Čiháková
Frontiers in Immunology, 2017 - Eosinophil-derived IL-4 drives progression of myocarditis to inflammatory dilated cardiomyopathy
Nicola L. Diny, G. Christian Baldeviano, Monica V. Talor, Jobert G. Barin, SuFey Ong, et al.
Journal of Experimental Medicine, 2017 - Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart
Nicola L. Diny, Xuezhou Hou, Jobert G. Barin, Guobao Chen, Monica V. Talor, et al.
European Journal of Immunology, 2016 - Collaborative Interferon-γ and Interleukin-17 Signaling Protects the Oral Mucosa from Staphylococcus aureus
Jobert G. Barin, Monica V. Talor, Julie A. Schaub, Nicola L. Diny, Xuezhou Hou, et al.
American Journal of Pathology, 2016 - Pathogenic IL-23 signaling is required to initiate GM-CSF-driven autoimmune myocarditis in mice
Lei Wu, Nicola L. Diny, SuFey Ong, Jobert G. Barin, Xuezhou Hou, et al.
European Journal of Immunology, 2016 - Natural killer cells limit cardiac inflammation and fibrosis by halting eosinophil infiltration
SuFey Ong, Davinna L. Ligons, Jobert G. Barin, Lei Wu, Monica V. Talor, et al.
American Journal of Pathology, 2015 - Ubiquitin-like protein ISG15 (Interferon-Stimulated Gene of 15 kDa) in host defense against heart failure in a mouse model of virus-induced cardiomyopathy
Anna Rahnefeld, Karin Klingel, Anett Schuermann, Nicola L. Diny, Nadine Althof, et al.
Circulation, 2014 - Genome-wide consequences of deleting any single gene
Xinchen Teng, Margaret Dayhoff-Brannigan, Wen-Chih Cheng, Catherine E. Gilbert, Cierra N. Sing, et al.
Molecular Cell, 2013
