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De'Broski Herbert, PhD
Professor
Tulane University

Due to an inherent fascination with parasitic helminthes, De’Broski R. Herbert earned a B.S. in Microbiology from Xavier University of Louisiana (1994) and a Ph.D. in Immunology from Thomas Jefferson Medical College (2000). His thesis work demonstrated a critical role for IL-5, B-1 lymphocytes, and eosinophils in host-protective immunity against Strongyloides stercoralis (J Immunol. 2000 Oct 15;165(8):4544-51).

As part of a life-long dream, De’Broski spent several years in South Africa to complete his post-doctoral training at the University of Cape Town in the laboratory of Frank Brombacher Ph.D. This resulted in seminal work that demonstrated IL-4/IL-13-driven alternative macrophage activation controls lethal immunopathology during Schistosoma mansoni infection (Immunity. 2004 May;20 (5):623-35).

Subsequently, he joined the laboratory of Fred. D. Finkelman M.D. and published multiple studies focused on the importance of IL-4/IL-13 in driving host-protection against parasitic helminthes through direct regulation of tissue macrophage function (J Immunol. 2010 Jun 1;184(11):6438-46) and mucosal epithelia (J Exp Med. 2009 Dec 21;206(13):2947-57).

As principal investigator of his independent laboratory at Cincinnati Children’s Research Foundation, his work focused upon elucidating mechanisms of innate Type 2 cytokine regulation by Trefoil factor family proteins (J Exp Med. 2012 Mar 12;209 (3):607-22) and immunosuppressivemacrophage subsets in the context of helminth infection and allergic inflammation (Eur J Immunol. 2011 Jul;41(7):2000-9,
Am J Pathol. 2012 May;180(5):2001-8).

As a Professor of Immunology, Department of Microbiology/Immunology, Tulane University School of Medicine, Dr. Herbert studies how IL-33, a key immune molecule, influences inflammation, tissue repair, and allergic diseases. His research reveals how myeloid-derived IL-33 drives type 2 immune responses, shaping how our bodies react to parasites, lung disease, and gut inflammation.

His recent work has uncovered how IL-33 can act as both an inflammatory trigger and a healing signal, offering new insights into treating asthma, allergies, and chronic inflammatory conditions.

Research Area(s):

Cancer
Immunology
Infectious Disease
Drug Discovery/Technology

Research Keywords:

# Regulatory Networks
# Immunity
# Inflammation
# Tissue Repair
# Mucosal Interface

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