This Administrative Core will mediate three functions. As part of the first function it will help coordinate the Principal Project, the Collaborative Project and the Pilot Project. At a fixed time on the first Monday of every month the project coordinator and the Investigators and Co-investigators of the three projects will meet face-to-face or by conference call at Massachusetts General Hospital to chart progress and coordinate studies and sample collection. These meetings will expand on ongoing regular monthly meetings currently being held. A second goal of this Core will be to make available tools of Human Immunology research to other investigators at MGH studying autoimmune disorders other than lgG4-Related Disease including Next Gen sequencing for repertoire, expertise with the Cytof, cell storage and profiling techniques. The ACE program coordinator will regularly inform the broader MGH community of the time and location of the monthly meetings and an hour will be set aside by the Principal Investigator to meet clinicians and other investigators at the MGH who seek to interact. These interactions will also facilitate some of the studies of the Principal Project on an unusual type of disease causing human T cell subset. The third goal of this Core and its coordinator will be to generate a portal for interaction with other ACEs and to share information on Immune repertoires, microbial community characteristics and eventually Immunochip data with other groups working across the country on autoimmunity, not necessarily restricted to other ACEs

Public Health Relevance

Coordinated Efforts will be required to better understand the underlying mechanisms causing human autoimmune diseases. This ACE involves investigators different departments at Massachusetts General Hospital and the Broad Institute of Harvard and MIT. Since many diseases utilize common mechanisms the exchange of information and ideas is crucial to progress.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
1U19AI110495-01
Application #
8732926
Study Section
Special Emphasis Panel (ZAI1)
Project Start
Project End
Budget Start
2014-05-01
Budget End
2015-04-30
Support Year
1
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199
Perugino, Cory A; Mattoo, Hamid; Mahajan, Vinay S et al. (2017) Emerging Treatment Models in Rheumatology: IgG4-Related Disease: Insights Into Human Immunology and Targeted Therapies. Arthritis Rheumatol 69:1722-1732
Maehara, Takashi; Mattoo, Hamid; Ohta, Miho et al. (2017) Lesional CD4+ IFN-?+ cytotoxic T lymphocytes in IgG4-related dacryoadenitis and sialoadenitis. Ann Rheum Dis 76:377-385
Mahajan, Vinay S; Pillai, Shiv (2016) Sialic acids and autoimmune disease. Immunol Rev 269:145-61
Wallace, Zachary S; Mattoo, Hamid; Mahajan, Vinay S et al. (2016) Predictors of disease relapse in IgG4-related disease following rituximab. Rheumatology (Oxford) 55:1000-8
Mahajan, Vinay S; Demissie, Ezana; Mattoo, Hamid et al. (2016) Striking Immune Phenotypes in Gene-Targeted Mice Are Driven by a Copy-Number Variant Originating from a Commercially Available C57BL/6 Strain. Cell Rep 15:1901-9
Azimi, Ehsan; Reddy, Vemuri B; Shade, Kai-Ting C et al. (2016) Dual action of neurokinin-1 antagonists on Mas-related GPCRs. JCI Insight 1:e89362
Mattoo, Hamid; Mahajan, Vinay S; Maehara, Takashi et al. (2016) Clonal expansion of CD4(+) cytotoxic T lymphocytes in patients with IgG4-related disease. J Allergy Clin Immunol 138:825-838
Yuen, Grace J; Demissie, Ezana; Pillai, Shiv (2016) B lymphocytes and cancer: a love-hate relationship. Trends Cancer 2:747-757
Wallace, Zachary S; Mattoo, Hamid; Carruthers, Mollie et al. (2015) Plasmablasts as a biomarker for IgG4-related disease, independent of serum IgG4 concentrations. Ann Rheum Dis 74:190-5
Della-Torre, Emanuel; Feeney, Eoin; Deshpande, Vikram et al. (2015) B-cell depletion attenuates serological biomarkers of fibrosis and myofibroblast activation in IgG4-related disease. Ann Rheum Dis 74:2236-43

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