Founded in 1958, the Allergy Fellowship Training program of the University of Cincinnati has received continuous approval by the American Council of Graduate Medical Education. Over the past 20 years the number of career scientists engaged in NIH funded research at the University of Cincinnati College of Medicine and the Cincinnati Children's Hospital Medical Center have increased in quality and numbers. In parallel, NIH funded grants for allergy, immunology and others have substantially increased to over $17.5 million in 2006. Due to a critical mass of NIH funded basic and clinical researchers, educators, core and clinical facilities creating an ideal academic and research environment, our program was awarded an A/I T32 training grant in 2004 to continue through 2009. This award enabled expansion of the Allergy Training Program to a three year experience offering two research tracks including: 1) basic research providing mentored laboratory bench experience and 2) a Clinical Translational track. NIH funded research programs are currently available in our Pediatric and Internal Medicine Allergy-Immunology sections fostering multiple collaborative programs, creating an excellent environment for preparing young physicians for careers in academic medicine and research. The program emphasizes training of physician scientists for careers in food allergy research and epidemiology of allergic disorders. During the initial five years of this T32, highly qualified physicians have been trained, producing favorable outcomes including the addition of two new junior faculty in the Departments of Internal Medicine and Pediatrics.

Public Health Relevance

In order to build upon our early success, we are resubmitting a renewal application for this T32 and request continuation of our current funding of two training slot per year. Adequate human and physical resources exist at our institutions to justify our request both designated for postdoctoral MD or MD, Ph.D. candidates. The impact of this T32 program on public health will to be substantial in that physician scientists completing our program will make important contributions in defining allergic disease mechanisms and new treatments.

National Institute of Health (NIH)
National Institute of Allergy and Infectious Diseases (NIAID)
Institutional National Research Service Award (T32)
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Study Section
Allergy & Clinical Immunology-1 (AITC)
Program Officer
Prograis, Lawrence J
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University of Cincinnati
Internal Medicine/Medicine
Schools of Medicine
United States
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Nanda, Maya K; LeMasters, Grace K; Levin, Linda et al. (2016) Allergic Diseases and Internalizing Behaviors in Early Childhood. Pediatrics 137:
Davis, Benjamin P; Epstein, Tolly; Kottyan, Leah et al. (2016) Association of eosinophilic esophagitis and hypertrophic cardiomyopathy. J Allergy Clin Immunol 137:934-936.e5
Lindsley, Andrew W; Saal, Howard M; Burrow, Thomas A et al. (2016) Defects of B-cell terminal differentiation in patients with type-1 Kabuki syndrome. J Allergy Clin Immunol 137:179-87.e10
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Vrazo, Alexandra C; Hontz, Adrianne E; Figueira, Sarah K et al. (2015) Live cell evaluation of granzyme delivery and death receptor signaling in tumor cells targeted by human natural killer cells. Blood 126:e1-e10
Codispoti, Christopher D; Bernstein, David I; Levin, Linda et al. (2015) Early-life mold and tree sensitivity is associated with allergic eosinophilic rhinitis at 4 years of age. Ann Allergy Asthma Immunol 114:193-198.e4
Nanda, Maya K; Elenburg, Shelby; Bernstein, Jonathan A et al. (2015) Clinical features of pediatric hereditary angioedema. J Allergy Clin Immunol Pract 3:392-5
Codispoti, Christopher D; LeMasters, Grace K; Levin, Linda et al. (2015) Traffic pollution is associated with early childhood aeroallergen sensitization. Ann Allergy Asthma Immunol 114:126-33
Kumar, Sudhir; Khodoun, Marat; Kettleson, Eric M et al. (2014) Glyphosate-rich air samples induce IL-33, TSLP and generate IL-13 dependent airway inflammation. Toxicology 325:42-51
Li, Jinzhu; Figueira, Sarah K; Vrazo, Alexandra C A et al. (2014) Real-time detection of CTL function reveals distinct patterns of caspase activation mediated by Fas versus granzyme B. J Immunol 193:519-28

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