Daniella M. Schwartz, MD
- University of Pittsburgh, Department of Medicine, Division of Rheumatology and Clinical Immunology
- University of Pittsburgh, Department of Immunology
- Laboratory of Allergic Diseases, NIAID, NIH (Research Collaborator)
- Assistant Director, Microbiology and Immunology Departments (MID) Scholars Program
Education & Training
- Postdoctoral Fellowship, NIAMS, Molecular Immunology and Inflammation Branch, 2018
- Fellowship, Clinical Rheumatology, NIAMS, National Institutes of Health, 2015
- Chief Medical Resident, Virginia Commonwealth University, 2012
- Residency, Internal Medicine, Virginia Commonwealth University, 2011
- Wake Forest University School of Medicine, MD, Medicine, 2007
- Rice University, BA, Biochemistry and French, 2001
Research Interest Summary
Research Interests
My lab investigates mechanisms of immune dysregulation, with a focus on genetic and epigenetic regulation of immune cells and cytokines. Autoimmune and autoinflammatory diseases affect over 10 million people in the US alone, many of whom do not respond to currently approved therapies. Understanding the mechanisms driving autoimmunity and autoinflammation can help develop better treatments. We believe that rare diseases offer a "window" into other diseases, allowing us to understand basic mechanisms driving inflammatory disease risk and development. Our group seeks to improve the basic understanding of human immune dysregulation diseases using “pathway to phenotype” approaches that are rooted in understanding the molecular drivers of immune activation. In contrast to phenotype-based approaches, that characterize diseases based on clinical presentation and then explore molecular mechanisms, we take a “phenotype-agnostic” approach that seeks to start with a molecular immunologic phenotype and understand the resulting disease spectrum in subjects with dysregulation of specific pathways.
Publications
Karri U, Harasimowicz M, Carpio Tumba M, Schwartz DM. The Complexity of Being A20: From Biological Functions to Genetic Associations. J Clin Immunol 2024 Mar:44(3):76.
Son A, Meylan F, Gomez-Rodriguez J, Kaul Z, Sylvester M, Falduto GH, Vazquez E, Haque T, Kitakule MM, Wang C, Manthiram K, Qi CF, Cheng J, Gurram RK, Zhu J, Schwartzberg P, Milner JD, Frischmeyer-Guerrerio PA, Schwartz DM. Dynamic chromatin accessibility licenses STAT5- and STAT6-dependent innate-like function of TH9 cells to promote allergic inflammation. Nat Immunol. 2023 Jun;24(6):1036-1048
Schwartz DM, Kitakule MM, Dizon BL, Gutierrez-Huerta C, Blackstone SA, Burma AM, Son A, Deuitch N, Rosenzweig S, Komarow H, Stone DL, Jones A, Nehrebecky M, Hoffmann P, Romeo T, de Jesus AA, Alehashemi S, Garg M, Torreggiani S, Montealegre Sanchez GA, Honer K, Souto Adeva G, Barron KS, Aksentijevich I, Ombrello AK, Goldbach-Mansky R, Kastner DL, Milner JD, Frischmeyer-Guerrerio P. Systematic evaluation of nine monogenic autoinflammatory diseases reveals common and disease-specific correlations with allergy-associated features. Ann Rheum Dis. 2021 Jun;80(6):788-795. doi: 10.1136/annrheumdis-2020-219137. Epub 2021 Feb 22.
Schwartz DM, Blackstone SA, Sampaio-Moura N, Rosenzweig S, Burma AM, Stone D, Hoffmann P, Jones A, Romeo T, Barron KS, Waldman MA, Aksentijevich I, Kastner DL, Milner JD, Ombrello AK. Type I interferon signature predicts response to JAK inhibition in haploinsufficiency of A20. Ann Rheum Dis. 2020 Mar;79(3):429-431. doi: 10.1136/annrheumdis-2019-215918. Epub 2019 Nov 25.
Schwartz DM, Farley TK, Richoz N, Yao C, Shih HY, Petermann F, Zhang Y, Sun HW, Hayes E, Mikami Y, Jiang K, Davis FP, Kanno Y, Milner JD, Siegel R, Laurence A, Meylan F, O'Shea JJ.Retinoic Acid Receptor Alpha Represses a Th9 Transcriptional and Epigenomic Program to Reduce Allergic Pathology. Immunity. 2019 Jan 15;50(1):106-120.e10. doi: 10.1016/j.immuni.2018.12.014..