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Contact Info

Calman Prussin, M.D.
Phone: 301-496-1306
Email: cprussin@niaid.nih.gov
Mail:
Building 10, Room 11C207
10 Center Drive
MSC 1881
Bethesda, MD 20892-1881

See Also

Laboratory of Allergic Diseases

Calman Prussin, M.D.

Chief, Lymphocyte Biology Unit
Tenure-Track Investigator


Dr. Prussin received his M.D. at the University of Southern California (USC) Keck School of Medicine and completed his internal medicine residency at Los Angeles County–USC Medical Center. Following a postdoctoral fellowship in the Laboratory of Cellular and Molecular Immunology at NIAID, he completed his allergy and immunology clinical fellowship at NIH (1991–1995). In 1996, Dr. Prussin joined the Laboratory of Allergic Diseases as head of the Clinical Allergy Unit. From 2000 to 2007, Dr. Prussin was the associate director of the NIH Allergy and Immunology Fellowship Training Program. In 2007, Dr. Prussin was named chief of the Lymphocyte Biology Unit.

Description of Research Program

chart showing reactions to food allergens
Food allergen-specific T-cell responses in eosinophilic GI disease, peanut anaphylaxis and non-allergic control subjects. Credit: NIAID

IgE-mediated immediate hypersensitivity and eosinophilic inflammation are the two major pathological processes that underlie allergic disease. Th2 cells and their signature cytokines, IL-4, IL-5, and IL-13, are necessary for both IgE and eosinophilia. Thus, understanding Th2 cell biology is of paramount importance in developing new treatments for allergic diseases. The major focus of our work is establishing the concept of Th2 cell heterogeneity: that distinct Th2 subpopulations exist, and these subsets have specific effector functions and roles in allergic disease pathogenesis. Current projects are aimed at characterizing the cellular and molecular biology of these Th2 subpopulations and their roles in allergic disease pathogenesis.

We utilize anaphylactic food allergy and eosinophilic gastrointestinal disorders (EGIDs) as allergic disease paradigms that are respectively IgE- and eosinophil-dominated-, and as such provide a unique insight into these two fundamental allergic processes. Current translational studies are focused on characterizing the role of food allergen-specific T cells in alternatively driving IgE-dominant versus eosinophil-dominant immunopathology. Recent work from our lab demonstrates that EGIDs are associated with a unique population of IL-5+ Th2 cells that are not found in conventional anaphylactic food allergy (Figure). These findings demonstrate heterogeneity within the Th2 subset, with different Th2 cells alternatively favoring IgE-mediated or eosinophil-dominant immunopathology. Current work is focused on further characterizing “pro-anaphylactic” and “pro-eosinophilic” Th2 cells in both human allergic disease and mouse models of food allergy.

Memberships

American Academy of Allergy, Asthma and Immunology (Fellow); International Eosinophil Society; U.S. Public Health Service Commissioned Officers Association

Editorial Board

Journal of Allergy and Clinical Immunology

Research Group Members

Yuzhi Yin, M.D. Ph.D.; Molly Balsley, Ph.D.; Bhaskar Upadhyaya, Ph.D.; Daniel Wansley, Ph.D.

Major Areas of Research

  • Th2 gene regulation and Th2 cell differentiation
  • Food allergy—pathogenesis and treatment
  • Eosinophilic gastrointestinal disease pathogenesis and treatment
  • Immunological therapy of allergic diseases

Clinical Research Protocols

Selected Recent Publications

To view a complete listing, visit PubMed.

Prussin C, Yin Y, Upadhyaya B. Th2 heterogeneity: Does function follow form? J Allergy Clin Immunol. 2010 Dec;126(6):1094-8.

Prussin C, Lee J, Foster B. Eosinophilic gastrointestinal disease and peanut allergy are alternatively associated with IL-5+ and IL-5- T(H)2 responses. J Allergy Clin Immunol. 2009 Dec;124(6):1326-32.

Foroughi S, Foster B, Kim N, Bernardino LB, Scott LM, Hamilton RG, Metcalfe DD, Mannon PJ, Prussin C. Anti-IgE treatment of eosinophil-associated gastrointestinal disorders. J Allergy Clin Immunol. 2007 Sep;120(3):594-601.

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Last Updated July 08, 2011