Nathan Schuldt, PhD

Assistant Professor, Department of Pediatrics

Nathan Schuldt

Contact Info

Office Phone 612-626-4598

Fax 612-625-2199

Lab Phone 612-626-9684

Mailing Address:
Pediatric Rheumatology
campus code 2641
2101 6th Street SE,
2-200 WMBB
Minneapolis, MN 55455

Lab Address:
Center for Immunology
Wallin Medical Biosciences Building (WMBB), room 2-200
2101 6th St SE
Minneapolis, MN 55414

Additional Locations


Google Scholar

Postdoctoral Fellowship, Binstadt Lab, University of Minnesota Medical School, Minneapolis, MN

PhD, Genetics, Michigan State University, East Lansing, MI

BS/BA, Biology, University of Minnesota, Minneapolis, MN


Dr. Schuldt studied Biology at the University of Minnesota earning his BS degree in 2003. He then worked as a technologist at Viromed in the donor serology department before entering the Genetics Graduate Program at Michigan State University in 2007. At Michigan State Dr. Schuldt studied interactions between adenovirus and the immune system. It was here that Dr. Schuldt became fascinated with T cell immunology. Dr. Schuldt earned his PhD in Genetics in 2012 and joined the laboratory of Dr. Bryce Binstadt in the Center for Immunology at the University of Minnesota. Dr. Schuldt’s current research investigates how dual TCR expression alters thymic selection and T cell fate decisions to gain a better understanding of how tolerance breaks down leading to autoimmunity.


  • T cell biology
  • T cell subsets
  • T cell development
  • Dual TCR expression
  • Thymic selection
  • Autoimmunity
  • Type 1 Diabetes

Awards & Recognition

  • Basic Science Paper of the Year, Pediatrics Department, University of Minnesota (2018)
  • American Association of Immunologists Trainee Travel Award (2017)
  • 31st Annual PRESS Award, Pediatrics Department, University of Minnesota (2017)
  • 29th Annual PRESS Awards, Pediatrics Department, University of Minnesota (2015)
  • American Association of Immunologists Trainee Poster Award (2013)
  • Outstanding Genetics Graduate Student Award, Michigan State University (2011)
  • Genetics Program Travel Grant Award, Michigan State University (2011)
  • Graduate School Travel Grant Award, Michigan State University (2011)
  • Graduate School Research Enhancement Award, Michigan State University (2011)
  • S & S/Micro & Gen/COM/Fellowship, Michigan State University (2008)

Professional Associations

  • American Association for the Advancement of Science, 2012-present member
  • American Association of Immunologists, 2013-present member
  • American Association of Immunologists Public Policy Fellow, 2017-2018
  • University of Minnesota Center for Immunology (CFI) Postdoctoral Program, 2015-present
  • Michigan State University Genetics Graduate Program Student Organization, 2012 President


Research Summary/Interests

Multiple immune tolerance mechanisms prevent self-reactive T cells from becoming pathogenic. Autoimmunity occurs when these mechanisms break down. Thymic selection, also referred to as central tolerance, is the first prevention a self-reactive T cell encounters. During this process antigen recognizing T cell receptors (TCRs) are tested against various self-peptides, those that react too strongly are either deleted or shuttled into the regulatory T cell lineage. My research aims to understand how self-reactive T cells escape this process. 

One hypothesized method is through the expression of two different TCRs on a single T cells. An estimated 30% of all T cells express two functionally recombined TCRs. We hypothesize that this dual TCR expression can limit deletion and regulatory T cell commitment of strongly self-reactive T cells in the thymus. This could explain how self-reactive T cells escape the thymus and enter the periphery as pathogenic T cells. Dual TCR expression is hypothesized to play important roles in several other immune contexts including allo-responses in graft rejection, allergy, and protective immunity. We have developed new tools in our lab that allow us to detect and study dual TCR T cells in several immune contexts.


Cutting Edge: Dual TCR? Expression Poses an Autoimmune Hazard by Limiting Regulatory T Cell Generation.
Schuldt NJ, Auger JL, Spanier JA, Martinov T, Breed ER, Fife BT, Hogquist KA, Binstadt BA.
Journal of immunology (Baltimore, Md. : 1950). 2017; 199(1):33-38. NIHMSID: NIHMS872838
PMID: 28539428   PMCID: PMC5501482

Bi-Allelic TCR? or ? Recombination Enhances T Cell Development but Is Dispensable for Antigen Responses and Experimental Autoimmune Encephalomyelitis.
Schuldt NJ, Auger JL, Hogquist KA, Binstadt BA.
PloS one. 2015; 10(12):e0145762.
PMID: 26693713  PMCID: PMC4687847

Vaccines expressing the innate immune modulator EAT-2 elicit potent effector memory T lymphocyte responses despite pre-existing vaccine immunity.
Aldhamen YA, Seregin SS, Schuldt NJ, Rastall DP, Liu CJ, Godbehere S, Amalfitano A.
Journal of immunology (Baltimore, Md. : 1950). 2012; 189(3):1349-59. 
PMID: 22745373

Malaria vaccines: focus on adenovirus based vectors.
Schuldt NJ, Amalfitano A.
Vaccine. 2012; 30(35):5191-8.
PMID: 22683663

Immunogenicity when utilizing adenovirus serotype 4 and 5 vaccines expressing circumsporozoite protein in naïve and adenovirus (Ad5) immune mice.
Schuldt NJ, Aldhamen YA, Godbehere-Roosa S, Seregin SS, Kousa YA, Amalfitano A.
Malaria journal. 2012; 11:209.
PMID: 22720732  PMCID: PMC3472263

Expression of the SLAM family of receptors adapter EAT-2 as a novel strategy for enhancing beneficial immune responses to vaccine antigens.
Aldhamen YA, Appledorn DM, Seregin SS, Liu CJ, Schuldt NJ, Godbehere S, Amalfitano A.
Journal of immunology (Baltimore, Md. : 1950). 2011; 186(2):722-32.
PMID: 21149608

Vaccine platforms combining circumsporozoite protein and potent immune modulators, rEA or EAT-2, paradoxically result in opposing immune responses.
Schuldt NJ, Aldhamen YA, Appledorn DM, Seregin SS, Kousa Y, Godbehere S, Amalfitano A.
PloS one. 2011; 6(8):e24147.
PMID: 21912619  PMCID: PMC3166157

Adenovirus capsid-display of the retro-oriented human complement inhibitor DAF reduces Ad vector-triggered immune responses in vitro and in vivo.
Seregin SS, Aldhamen YA, Appledorn DM, Hartman ZC, Schuldt NJ, Scott J, Godbehere S, Jiang H, Frank MM, Amalfitano A.
Blood. 2010; 116(10):1669-77. 
PMID: 20511542  PMCID: PMC2947391

A new adenovirus based vaccine vector expressing an Eimeria tenella derived TLR agonist improves cellular immune responses to an antigenic target.   Appledorn DM, Aldhamen YA, Depas W, Seregin SS, Liu CJ, Schuldt N, Quach D, Quiroga D, Godbehere S, Zlatkin I, Kim S, McCormick JJ, Amalfitano A. 
PloS one. 2010; 5(3):e9579. 
PMID: 20221448  PMCID: PMC2833191

CR1/2 is an important suppressor of Adenovirus-induced innate immune responses and is required for induction of neutralizing antibodies.
Seregin SS, Aldhamen YA, Appledorn DM, Schuldt NJ, McBride AJ, Bujold M, Godbehere SS, Amalfitano A.
Gene therapy. 2009; 16(10):1245-59. NIHMSID: NIHMS113191
PMID: 19554032  PMCID: PMC4039027

Transient pretreatment with glucocorticoid ablates innate toxicity of systemically delivered adenoviral vectors without reducing efficacy.
Seregin SS, Appledorn DM, McBride AJ, Schuldt NJ, Aldhamen YA, Voss T, Wei J, Bujold M, Nance W, Godbehere S, Amalfitano A.
Molecular therapy: the journal of the American Society of Gene Therapy. 2009; 17(4):685-96.
PMID: 19174760  PMCID: PMC2835110

Complex interactions with several arms of the complement system dictate innate and humoral immunity to adenoviral vectors.
Appledorn DM, McBride A, Seregin S, Scott JM, Schuldt N, Kiang A, Godbehere S, Amalfitano A.
Gene therapy. 2008; 15(24):1606-17.
PMID: 18615115