Nathan Schuldt, PhD

Assistant Professor, Department of Pediatrics

Nathan Schuldt

Contact Info

schu1048@umn.edu

Office Phone 612-626-4598

Fax 612-625-2199

Lab Phone 612-626-9684

Office Address:
Pediatric Rheumatology
2-200 WMBB
2101 6th Street SE
Minneapolis, MN 55414

Mailing Address:
Pediatric Rheumatology
2-200 WMBB
2641G (Campus Delivery Code)
2101 6th Street SE
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

ResearchGate

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

Summary

Nathan Schuldt, PhD, is an Assistant Professor in the Department of Pediatrics in the Division of Pediatric Rheumatology. Dr. Schuldt runs a laboratory at the University of Minnesota’s Center for Immunology. His laboratory investigates the origins of autoimmune diseases like type 1 diabetes (T1D) and multiple sclerosis (MS). Dr. Schuldt has particular interest in T cell development, tolerance, and fate decisions.

Dr. Schuldt earned his PhD in Genetics in 2012 at Michigan State University training in the laboratory of Andrea Amalfitano, DO, PhD. His graduate studies focused on the interactions between adenovirus and the immune system with the goal of improving adenovirus-based vectors for gene therapy and vaccination. He joined the University of Minnesota Center for Immunology in 2012 as a Postdoctoral Fellow. 

Expertise

  • 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

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 and initiate autoimmune disease.

One hypothesized method is through the expression of two different TCRs on a single T cells. An estimated 10-20% 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.

A second area of interest for the lab is neonatal immune development. At birth, the adaptive immune system is underdeveloped and may function differently than that of adults. As a result, infections are common in neonates and infants. The Schuldt Lab has begun a collaboration to investigate how early microbial exposure influences the development of adaptive immunity. Improved understanding of neonatal adaptive immunity could lead to improved vaccine platforms.

Publications

Noninvasive ultrasound stimulation of the spleen to treat inflammatory arthritis.
Zachs DP, Offutt SJ, Graham RS, Kim Y, Mueller J, Auger JL, Schuldt NJ, KaiserCRW, Heiller AP, Dutta R, Guo H, Alford JK, Binstadt BA, Lim HH.Nat Commun. 2019 Mar 12;10(1):951. doi: 10.1038/s41467-019-08721-0.PMID: 30862842 PMCID: PMC6414603

Dual TCR T Cells: Identity Crisis or Multitaskers?
Schuldt NJ, Binstadt BA.
J Immunol. 2019 Feb 1;202(3):637-644. doi: 10.4049/jimmunol.1800904. Review.
PMID:30670579

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: NIHMS872838PMID: 28539428PMCID: 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: NIHMS113191PMID: 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