Abstract

The Mouse Genetic Core (Core A) is an integral part of this effort, as it has in the past and hopefully in the future will support the work of the Program Project Grant by providing complex knockout mice and BAC transgenic mouse strains will serve as a repository for all newly developed mouse strains. Core A has three Specific Aims: #1 To generate novel knockout mouse strains, which will support P#1 and P#2 and based upon interactions with human studies in P#2 and P#3. #2 To generate transgenic mice based BAC clones and mutant BAC clones obtained by multi-step recombineering, which will support P#1 and P#2 and based upon interactions with human studies in P#2 and P#3. #3 To support the mutant mouse activities in P#1 and P#2, and to maintain the transgenic and knockout mouse strains used by P#1, P#2 and to facilitate treatment studies as guided by P#3.

Public Health Relevance

Results of these studies should lead to 1) better diagnostic tools to complement currently used indexes, 2) reliable and specific biomarkers to monitor and hopefully predict disease activity and 3) novel treatment protocols for SLE patients to replace or add to immunosuppressive drugs.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
4P01AI065687-10
Application #
9109559
Study Section
Special Emphasis Panel (ZAI1)
Project Start
Project End
Budget Start
2016-08-01
Budget End
2017-07-31
Support Year
10
Fiscal Year
2016
Total Cost
Indirect Cost

  Institution

Name
Beth Israel Deaconess Medical Center
Department
Type
DUNS #
071723621
City
Boston
State
MA
Country
United States
Zip Code

  Publications

Cuenca, Marta; Puñet-Ortiz, Joan; Ruart, Maria et al. (2018) Ly9 (SLAMF3) receptor differentially regulates iNKT cell development and activation in mice. Eur J Immunol 48:99-105
Comte, Denis; Karampetsou, Maria P; Kis-Toth, Katalin et al. (2017) Brief Report: CD4+ T Cells From Patients With Systemic Lupus Erythematosus Respond Poorly to Exogenous Interleukin-2. Arthritis Rheumatol 69:808-813
Comte, Denis; Karampetsou, Maria P; Yoshida, Nobuya et al. (2017) Signaling Lymphocytic Activation Molecule Family Member 7 Engagement Restores Defective Effector CD8+ T Cell Function in Systemic Lupus Erythematosus. Arthritis Rheumatol 69:1035-1044
Sage, Peter T; Ron-Harel, Noga; Juneja, Vikram R et al. (2016) Suppression by TFRcells leads to durable and selective inhibition of B cell effector function. Nat Immunol 17:1436-1446
Karampetsou, Maria P; Comte, Denis; Kis-Toth, Katalin et al. (2016) Decreased SAP Expression in T Cells from Patients with Systemic Lupus Erythematosus Contributes to Early Signaling Abnormalities and Reduced IL-2 Production. J Immunol 196:4915-24
Cuenca, Marta; Romero, Xavier; Sintes, Jordi et al. (2016) Targeting of Ly9 (CD229) Disrupts Marginal Zone and B1 B Cell Homeostasis and Antibody Responses. J Immunol 196:726-37
Kis-Toth, Katalin; Comte, Denis; Karampetsou, Maria P et al. (2016) Selective Loss of Signaling Lymphocytic Activation Molecule Family Member 4-Positive CD8+ T Cells Contributes to the Decreased Cytotoxic Cell Activity in Systemic Lupus Erythematosus. Arthritis Rheumatol 68:164-73
Comte, Denis; Karampetsou, Maria P; Kis-Toth, Katalin et al. (2016) Engagement of SLAMF3 enhances CD4+ T-cell sensitivity to IL-2 and favors regulatory T-cell polarization in systemic lupus erythematosus. Proc Natl Acad Sci U S A 113:9321-6
McArdel, Shannon L; Brown, Daniel R; Sobel, Raymond A et al. (2016) Anti-CD48 Monoclonal Antibody Attenuates Experimental Autoimmune Encephalomyelitis by Limiting the Number of Pathogenic CD4+ T Cells. J Immunol 197:3038-3048
McArdel, Shannon L; Terhorst, Cox; Sharpe, Arlene H (2016) Roles of CD48 in regulating immunity and tolerance. Clin Immunol 164:10-20

Showing the most recent 10 out of 58 publications