Major Areas of Research
- Identifying the molecular and epigenetic mechanisms underlying human T helper 9 lineage identity and function
- Identifying the mechanisms by which human T helper 9 cells promote end-organ pathology in patients with psoriasis and other systemic autoimmune diseases
- Investigation of cellular and molecular pathways responsible for the symptoms characteristic of haploinsufficiency of A20 (HA20) and related diseases
Diseases of immune activation are common and devastating, affecting up to 15% of the U.S. population and causing severe morbidity. Although identifying and targeting pathogenic cytokines has revolutionized disease treatment, many syndromes are treatment-refractory due to an incomplete understanding of the factors driving pathology. Our group seeks to improve the basic understanding of human immune activation by investigating relationships between allergic inflammation and autoimmune/autoinflammatory disorders. Notably, allergic factors have historically been thought to suppress these diseases, but recent evidence implicates allergic cells and cytokines as critical drivers of autoimmune pathology. We therefore aim to dissect the regulation and roles of allergy-associated cytokines in the context of autoimmune and autoinflammatory disease, using a multifaceted approach that combines mouse models with studies involving human patients.
Dr. Schwartz graduated with a B.A. in Biochemistry and French from Rice University and received an M.D. from the Wake Forest University School of Medicine in 2007. She completed her internal medicine residency training at Virginia Commonwealth University in 2010, after which she served as a chief medical resident. She completed a fellowship in clinical rheumatology at the National Institute of Arthritis and Musculoskeletal and Skin Diseases and was subsequently promoted to Metzger Scholar in Translational Research, where she did a postdoctoral fellowship in the lab of Dr. John O’Shea. In 2018, she was recruited to the NIAID intramural research program as an assistant clinical investigator. Dr. Schwartz was a recipient of the American Society of Clinical Investigation Young Physician Scientist Award in 2020.
Aarohan Burma, B.S., postbaccalaureate fellow; Aran Son, Ph.D., Biologist; Daniella Schwartz, M.D., Assistant Clinical Investigator; Moses Kitakule, B.S., Postbaccalaureate fellow; Sarah Blackstone, B.S., postbaccalaureate fellow
Schwartz DM, Blackstone SB, 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.
Schwartz DM, Burma AM, Kitakule MM, Luo Y, Mehta NN. T Cells in Autoimmunity-Associated Cardiovascular Diseases. Front Immunol. 2020 Oct 7;11:588776.
Schwartz DM, Farley T, 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.
Ahuja M*, Schwartz DM*, Tandon M, Son A, Zeng M, Swaim W, Eckhaus M, Hoffman V, Cui Y, Xiao B, Worley PF, Muallem S. Orai1-Mediated Antimicrobial Secretion from Pancreatic Acini Shapes the Gut Microbiome and Regulates Gut Innate Immunity. Cell Metab. 2017 Mar 7;25(3):635-646.
Zhou Q*, Wang H*, Schwartz DM, Stoffels M, Park YH, Zhang Y, Yang D, Demirkaya E, Takeuchi M, Tsai WL, Lyons JJ, Yu X, Ouyang C, Chen C, Chin DT, Zaal K, Chandrasekharappa SC, Hanson EP, Yu Z, Mulikin JC, Hasni SA, Wertz IE, Ombrello AK, Stone DL, Hoffmann P, Jones A, Barham BK, Leavis HL, van Royen-Kerkof A, Sibley C, Batu ED, Gul A, Siegel FM, Boehm M, Milner JD, Ozen S, Gadina M, Chae J, Laxer RM, Kastner DL, Aksentijevich I Loss-of-function mutations in TNFAIP3 leading to A20 haploinsufficiency cause an early-onset autoinflammatory disease. Nat Genet. 2016 Jan;48(1):67-73.
*authors contributed equally