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Dr. Jian Zhang’s Laboratory Staff Wins Multiple Presentation and Travel Awards

February 19, 2020

Na Tang
Ms. Na Tang has been awarded an American Association of Immunologists (AAI) Trainee Travel Award to present her research findings on how E3 ubiquitin ligase Cbl-b regulates pathogenic Th17 responses and the development of experimental autoimmune encephalomyelitis (EAE).  Ms. Tang is a Visiting Scholar in the laboratory of Dr. Jian Zhang. Utilizing adoptive transfer and cell type-specific Cblb knockout strains, she showed that Cbl-b expression in macrophages but not T cells or dendritic cells (DCs) restrains the generation of pathogenic Th17 cells and the development of EAE. Cbl-b inhibits the production of IL-6 by macrophages induced upon signaling via C-type lectin receptors, which directs T cells to generate pathogenic Th17 cells. The title of her abstract is “E3 Ubiquitin Ligase Cbl-b Restrains Priming of Pathogenic Th17 Cells via Inhibiting IL-6 Production by Macrophages”.
 

Patrick Nuro-Gyina
Mr. Patrick Nuro-Gyina has been awarded an American Association of Immunologists (AAI) Trainee Travel Award to present his research findings on HECT E3 Nedd4 in anti-fungal innate immunity.  Patrick is a Graduate Research Associate in Dr. Jian Zang’s laboratory and is working on how HECT E3 ubiquitin ligase Nedd4 controls anti-fungal innate immunity. He found that Nedd4 expression in myeloid cells is crucial for C-type lectin receptor (CLR)-mediated innate immune response against systemic C. albicans infection. The title of his abstract is “E3 Ubiquitin Ligase Nedd4 Is Essential for Anti-fungal Innate Immune Response”.
 

Chengkai Yan
Mr. Chengkai Yan has been awarded an American Association of Immunologists (AAI) Trainee Travel Award to present his research findings on the role of C-type lectin receptor Dectin-1 in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis.  Mr. Yan is a Visiting Scholar in the laboratory and is working on how Dectin-1 regulates the susceptibility of mice to EAE. He surprisingly found that mice deficient for Dectin-1 develop severe EAE. The heightened EAE severity observed in Dectin1–/– mice correlates with an increased Th17 response in the draining lymph nodes. Further analysis showed that Clec7a–/– mice have reduced regulatory CD8+ T cells, which have been shown to suppress EAE development.  The title of his abstract is “C-Type Lectin Receptor Dectin-1 Suppresses the Development of Experimental Autoimmune Encephalomyelitis”.
 

Monisha Mittal
Ms. Monisha Mittal has been awarded an American Association of Immunologists (AAI) Trainee Travel Award to present her research findings on how cGAS, a cytosolic DNA sensor regulates the development of EAE, and Th1/Th17 responses.  Monisha is a student in the Pathology M.S. Graduate Program.  She is currently working on how a cytosolic DNA sensor controls EAE development. She found that mice deficient for cGAS develop ameliorated EAE. Further studies suggest that cGAS expression in innate immune cells may indirectly regulate pathogenic Th1/Th17 responses during EAE induction.  The title of her abstract is titled “Cyclic GMP-AMP Synthase Regulates the Development of Experimental Autoimmune Encephalomyelitis”.


Hui Guo, MPA, a Research Specialist in Dr. Jian Zang’s laboratory was selected to give an oral presentation on the crucial role Type 2 innate lymphoid cells (ILC2) play in driving allergic airway inflammation, with an emphasis on the how ubiquitin ligases might regulate ILC2 development. Using various Cbl-b gene-targeted mouse strains, she showed that Cbl-b inhibits the development of ILC2 and ILC2-mediated airway inflammation by targeting ST2, an IL33 receptor, for ubiquitination and lysosome-mediated degradation. The title of her abstract is titled “E3 Ubiquitin Ligase Cbl-b Inhibits Type 2 Innate Lymphoid Cell Development by Targeting ST2 for Ubiquitination”.