Faculty & Staff
Stephen C. Dreskin, MD, PhD - Professor of Medicine and Immunology
Division of Allergy & Clinical Immunology
Director, University of Colorado Allergy, Immunology and Rheumatology Practices
Co-director, University of Colorado/National Jewish - Allergy/Clinical Immunol. training program
Medical Director & Clinical Consultant, Clinical Immunol./Flow Cytometry Lab, ClinImmune Labs
Assistant Medical Director, Colorado Cord Blood Bank, ClinImmune Labs
4200 East Ninth Ave, B164
Denver, CO 80262
Phone: (303) 315 6979 (Research Office)
Fax: (303) 315 7642 (Research Fax)
(See below for patient appointment contact info)
Stephen.Dreskin@uchsc.edu
- Education:
- 1971 BA (Biochemistry) University of Pennsylvania
- 1976 PhD (Physiology) Emory University
- 1977 MD (Medicine) Emory University
- 1977-78 Internship (Internal Medicine) University of California-Davis
- 1978-80 Residency (Internal Medicine) University of California-Davis
- 1981-85 Fellowship - National Institute of Allergy & Infections Diseases (NIAID), NIH, Bethesda, MD
- Board Certification:
- 1980 Internal Medicine
- 1983 Allergy and Immunology
- 1990 Diagnostic Laboratory Immunology
- Areas of Clinical Interest:
- Severe allergic reactions, severe food allergies
- Chronic Urticaria
- Angioedema
- Anaphylaxis
- Mastocytosis
- Asthma and Rhinitis
- Allergic Reactions to Vaccines
- Clinic Location:
- University of Colorado Allergy, Immunology and Rheumatology Practice
1635 N. Ursula St.
4th Floor, Anschutz Outpatient Pavilion
Aurora, CO 80010
Fax 720-848-1947 - Clinic Days:
- These are teaching clinics. Dr. Dreskin does not have a "private" clinic. Often, patients will first be evaluated by an MD who is taking subspecialty training in Allergy and Immunology. Dr. Dreskin can be requested to be the "Attending of Record".
- Dr. Dreskin is in clinic most Monday afternoons, Thursday mornings, and Friday mornings.
- Appointment Contact:
- 720-848-1940 (Call for appointments) 720-848-1947 (FAX for patient info)
- Research Interests:
-
Molecular basis of peanut allergy
-
Study of functional IgE-allergen interactions as they pertain to food allergies
-
Molecular basis of chronic urticaria
The primary effort in the Dreskin laboratory is to understand the effector activity of peanut allergens (funded by the National Institutes of Allergy and Infectious Diseases, NIH RO1AI052164). Allergic reactions to peanuts occur because susceptible individuals have an aberrant response to peanuts by producing a plasma protein, IgE, that binds to the high affinity receptor for IgE on mast cells and basophils. This receptor-bound IgE can be cross-linked by specific peanut proteins, called allergens, leading to a severe allergic reaction. Nine peanut proteins have been identified as allergens because they bind IgE from allergic individuals. Three of these, Ara h 1, Ara h 2, and Ara h 3 are called the major peanut allergens based on their ability to bind IgE on Western blots, to interact with IgE in RAST-inhibition assays, and to have measurable activity as assessed by in vitro and/or in vivo functional assays. Based on our work and the work of others, we now know that Ara h 2 is the most potent of these allergens. We have championed the concept of defining the clinically most important allergens based on potency in functional assays that we have helped to develop. Our newest data examining the allergenicity of peanut extracts that have been specifically depleted of Ara h 2 demonstrate strongly that, for severely peanut allergic patients, the activity of Ara h 2 does not account for the majority of the allergenic activity of peanuts. Using conventional chromatography combined with proteomics we propose to identify other important peanut allergens. We propose to extend our efforts to define quantitatively the major peanut allergens by combining our functional assays with the power of proteomics. In doing this we will define in molecular detail the peanut allergens most greatly responsible for mast cell activation in peanut allergic patients. We will test our in vitro findings in vivo using a mouse model of peanut allergy. This approach, in which we will definitively identify the most potent major allergens in peanuts, has the potential to completely change our thinking as to which peanut allergens are the most important for allergic reactions in specific patients.
Secondary efforts in the Dreskin laboratory include an ongoing-study of the genetics of peanut allergy (funded by the Food Allergy and Anaphylaxis Network) and the molecular basis of Urticaria (funded by institutional funds).
- Research Team:
- Harry Porterfield, BS
Syed Shahzad Mustafa, MD
Ojas Patel, MD
Darcy Schlichting, RN
Active Collaborators at University of Colorado Denver:
Heather Thompson, PhD
- Select Recent Publications:
- Robert A. McDermott, Harry Porterfield, Rabab El Mezayan, Darcy Schlichting, Kirk C. Hansen, Mark Duncan, Benjamin Solomon, Michael Simpson, Ronald Harbeck, Stephen C. Dreskin. Successful Removal of Ara h 2 from a Crude Peanut Extract Yields Minimal Change in Allergenicity, In press, Clinical and Experimental Allergy, 2007.
Dreskin, SC: Genetics of Food Allergy, Current Allergy & Asthma Reports, 6: 58-64, 2006.
Yasnowsky KM, Dreskin SC, Efaw B, Schoen D, Vedantahan PK, Alam R, and Harbeck R. Chronic Urticaria Sera Increase Basophil CD203c Surface Expression. J Allergy and Clin Immunol, 117: 1430-1434, 2006.
Palmer GW, Dibbern DA, Jr., Burks AW, Bannon GA, Bock SA, Porterfield, HS McDermott RA, and Dreskin SC. Comparative Potency of Ara h 1 and Ara h 2 in Immunochemical and Functional Assays of Allergenicity. Clinical Immunology, 115:302-312, 2005.
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Site Last Updated: 03/26/08