Overview

Dr. Siracusa received his doctorate in 2008 from Johns Hopkins University where his work focused on
understanding how hookworm-induced pulmonary inflammation is regulated by alveolar macrophages.
Following his time at Johns Hopkins, Dr. Siracusa continued his training at the University of Pennsylvania
where he made seminal discoveries defining the initiation and regulation of innate immune responses following
Trichinella and Trichuris infections. In 2014 Dr. Siracusa was recruited to the Center for Immunity and
Inflammation at Rutgers New Jersey Medical School as the Universities first Chancellor Scholar. Since joining
Rutgers, Dr. Siracusa has established a successful NIH-funded research program that has made fundamental
discoveries defining the diverse roles that granulocytes and neuroimmune interactions play in regulating
helminth-induced inflammation. Dr. Siracusa is also the president and founder of NemaGen Discoveries, a
biotech start-up company that develops novel therapeutics based on pathways discovered while studying
host-parasite interactions.

POSITIONS
2014-2021: Assistant Professor, Dept. of Medicine, Rutgers New Jersey Medical School
2021-present: Associate Professor, Dept. of Medicine, Rutgers New Jersey Medical School
2021-present: Director of the Research Support Core, Rutgers New Jersey MeMedical School

2021-present: Standing member of the NIH Innate Immunity and Inflammation Study Section

Education

PHD, 2008, John Hopkins University, Bloomberg School of Public Health, Baltimore, MD
BS, 2000, Merrimack College, North Andover MA

Curriculum Vitae

View CV

Relevant Publications

Peng J, Sy CB, Ponessa JJ, Lemenze AD, Hernandez CM, Inclan-Rico JM, Sawhney A, Federman HG, Chavan K, Espinosa V, Kotenko SV, Rivera A, Siracusa MC. Monocytes maintain central nervous system homeostasis following helminth-induced inflammation. PNAS. 2022 Sep 13;119(37). (PMID 36070344)

Inclan-Rico JM, Ponessa JP, Valero-Pacheco N, Hernandez CM, Sy CB, Lemenze AD, Beaulieu AM and Siracusa MC. Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition. Nature Immunology. 2020 Oct; 21(10):1181-1193. (PMID 32807942)

Inclan-Rico JM, Hernandez CM, Henry EK, Federman HG, Sy CB, Ponessa JP, Lemenze AD, Joseph N, Soteropoulos P, Beaulieu AM, Yap GS and Siracusa MC. Trichinella Spiralis-Induced Mastocytosis and Erythropoiesis Are Simultaneously Supported by a Bipotent Mast Cell/Erythrocyte Precursor Cell. PLOS Pathog. 2020 May 18;16(5):e1008579. (PMID 32421753)

Henry EK, Sy CB, Inclan-Rico JM, Channy SS, Dwyer DF, Soteropoulos P, Rivera A, Siracusa MC. Carbonic anhydrase enzymes regulate mast cell-mediated inflammation. Journal of Experimental Medicine. 2016 Aug 22; 213(9):1663-73. (PMID 27526715)

Siracusa MC, Hill DA, Ruymann KR, Tait Wojno ED, Artis D, and Spergel JM. Omalizumab therapy is associated with reduced circulating basophil populations in asthmatic children. Allergy. 2014 May; 69(5):674-7. (PMID 24611974)

Siracusa MC, Saenz SA, Tait Wojno ED, Kim BS, Osborne LC, Ziegler C, Benitez AJ, Ruymann KR, Farber DL, Sleiman PM, Hakonarson H, Cianferoni A, Wang ML, Spergel JM, Comeau MR, and Artis D. TSLP-mediated extramedullary hematopoiesis promotes allergic inflammation. Immunity. 2013 Dec 12; 39(6):1158-70. (PMID 24332033)

Siracusa MC, Saenz SA, Hill DA, Kim BS, Headley MB, Doering TA, Wherry EJ, Jessup HK, Siegel LA, Kambayashi T, Dudek EC, Kubo M, Cianferoni A, Spergel JM, Ziegel SF, Comeau MR, and Artis D. TSLP promotes interleukin-3-independent basophil haematopoiesis and type 2 inflammation. Nature. 2011 Aug 14; 477(7363):229-33. (PMID: 21841801)

Inclan-Rico JM, Ponessa JJ, Siracusa MC. Contributions of innate lymphocytes to allergic responses. Curr Opin Allergy Clin Immunol. 2019 Apr;19(2):175-184. (PMID: 30672750)

Henry EK, Inclan-Rico JM, Siracusa MC. Type 2 cytokine responses: regulating immunity to helminth parasites and allergic inflammation. Current Pharmacologic Reports. 2017 Dec;3(6)346:359. (PMID 29399438)

Sy CB, Siracusa MC. The Therapeutic Potential of Targeting Cytokine Alarmins to Treat Allergic Airway Inflammation. Frontiers in Physiology. 2016 Jun 14;7:214. (PMID 27378934)

Areas Of Interest

Inflammation

Allergic inflammation

Hematopoiesis

Mucosal Immunology

Parasitology

Course List

EDUC6100K

Foundations of Body Systems

Innate Immune regulation of antihelminth immunity

NIH RO1 1R01AI123224
Innate immune regulation of helminth-induced inflammation. The goal of this study is to define the
contributions of mast cells and basophils to the development of anti-helminth immunity.

NIH RO1 1R01AI131634
Protective and pathologic functions of macrophages induced by helminths. The goal of this study is to
define the contributions and cooperative mechanisms through which specialized innate cells and
macrophages promote protective immunity to gastrointestinal helminths.

NIH RO1 1R01AI151599
Neuropeptide regulation of antihelminth immunity. The goal of this study is to define how stimulatory
and inhibitory neuropeptides counterbalance each other to regulate antihelmith immunity.



TH2 cytokine responses are required for immunity to helminth parasites and are also responsible for the
detrimental inflammation associated with allergies and asthma. The global prevalence of soil transmitted
helminth infections is currently estimated at two billion individuals infected worldwide, with an estimated
one billion people infected with Trichuris alone. Helminth infections can lead to significant malnutrition,
growth retardation and long-term disability. In addition, infections of live stock populations in endemic
areas exert enormous economic burdens on the local communities. Given the global prevalence of
helminth infections coupled with the pandemic of allergic diseases in industrialized countries, it is critical
to gain a better understanding of the pathways that control TH2 cytokine-mediated immunity and
inflammation. CD4+ TH2 cells produce IL-4, IL-5, IL-9 and IL-13, and their development is dependent
on IL-4R, STAT6 and GATA3. In addition, B cells activated in the context of a TH2 cytokine response
primarily class switch to produce antigen-specific IgG1 and IgE. Type 2 cytokine-driven inflammation in
tissues results in goblet cell hyperplasia, mucus production, increased smooth muscle contractility, and
the influx of granulocyte populations. Despite significant developments in our understanding of the
pathways that control the differentiation and regulation of TH2 cells, the molecular and cellular pathways
that initiate helminth- or allergen-specific TH2 cell responses remain poorly defined. The focus of my
research is to definitively determine the contributions of innate immune cells such as basophils, mast
cells and macrophages on the development of type 2 cytokine responses.