In this program on lupus pathogenesis, we seek to understand the pathways that drive autoimmunity. The Research Technology Core (Core 1) is dedicated to providing standardized means for the study of these B cell and antibody responses, and for investigations of the host relationship with commensal bacteria in the gut. The Core will provide services that have customized to the needs of each of the Projects. Through centralization of these facilities, we will provide services that provide economies of scale and efficiency. These methods are state-of-the-art and are otherwise not available from NYU Core facilities or from commercial vendors. The Research Technology Core will perform already validated assays in four areas: i) Autoantibody surveys from serum and fecal samples. ii) Isolation of fecal bacteria coated in the bowel by endogenously produced IgA. iii) Microbiome analyses by 16S rRNA methods by Next Generation Sequencing. iv) Large-scale BCR transcript repertoire libraries. Herein, we will support studies for all three Projects of the contributions of specific antibody/B-cell clones from the initial breach of immune tolerance, and in the transition from preclinical to overt clinical disease, and during the later phase of ongoing disease process characterized by self-perpetuation of autoimmune disease.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Specialized Center (P50)
Project #
5P50AR070591-04
Application #
10004503
Study Section
Special Emphasis Panel (ZAR1)
Project Start
2017-09-22
Project End
2022-08-31
Budget Start
2020-09-01
Budget End
2021-08-31
Support Year
4
Fiscal Year
2020
Total Cost
Indirect Cost
Name
New York University
Department
Type
DUNS #
121911077
City
New York
State
NY
Country
United States
Zip Code
10016
Soni, Chetna; Reizis, Boris (2018) DNA as a self-antigen: nature and regulation. Curr Opin Immunol 55:31-37
Xu, Wanli; Luo, Zhenwu; Alekseyenko, Alexander V et al. (2018) Distinct systemic microbiome and microbial translocation are associated with plasma level of anti-CD4 autoantibody in HIV infection. Sci Rep 8:12863