Bio

Honors & Awards


  • Lubert Stryer Bio-X Stanford Interdisciplinary Graduate Fellowship, Stanford University (2015-2018)
  • Gabilan Stanford Graduate Fellowship in Science and Engineering, Stanford University (2012-2015)

Education & Certifications


  • Master of Science, Utrecht University, Infectious Diseases and Immunology (2011)
  • Bachelor of Science, Utrecht University, Pre-Med (2009)

Stanford Advisors


Service, Volunteer and Community Work


  • Volunteer, Maitland Cottage Home (July 1, 2008 - July 31, 2008)

    Assisted in surgeries and daily care of pediatric orthopedic patients in a hospital in Cape Town, South Africa.

    Location

    Maitland Cottage Home, Cape Town

  • Volunteer, Science is Elementary (4/1/2013)

    Teach STEM classes to elementary school students in the Bay Area.

    Location

    Bay Area, California, USA

Professional

Work Experience


  • Research Assistant, Stanford University (March 1, 2012)

    Location

    VA Palo Alto Health Care System

  • Research Trainee, Brigham and Women's Hospital, Harvard Medical School (February 14, 2011 - February 29, 2012)

    Location

    Brigham and Women's Hospital

Publications

Journal Articles


  • Orphan chemoattractant receptor GPR15 mediates dendritic epidermal T-cell recruitment to the skin EUROPEAN JOURNAL OF IMMUNOLOGY Lahl, K., Sweere, J., Pan, J., Butcher, E. 2014; 44 (9): 2577-2581
  • Autochthonous and dormant Cryptococcus gattii infections in Europe. Emerging infectious diseases Hagen, F., Colom, M. F., Swinne, D., Tintelnot, K., Iatta, R., Montagna, M. T., Torres-Rodriguez, J. M., Cogliati, M., Velegraki, A., Burggraaf, A., Kamermans, A., Sweere, J. M., Meis, J. F., Klaassen, C. H., Boekhout, T. 2012; 18 (10): 1618-1624

    Abstract

    Until recently, Cryptococcus gattii infections occurred mainly in tropical and subtropical climate zones. However, during the past decade, C. gattii infections in humans and animals in Europe have increased. To determine whether the infections in Europe were acquired from an autochthonous source or associated with travel, we used multilocus sequence typing to compare 100 isolates from Europe (57 from 40 human patients, 22 from the environment, and 21 from animals) with 191 isolates from around the world. Of the 57 human patient isolates, 47 (83%) were obtained since 1995. Among the 40 patients, 24 (60%) probably acquired the C. gattii infection outside Europe; the remaining 16 (40%) probably acquired the infection within Europe. Human patient isolates from Mediterranean Europe clustered into a distinct genotype with animal and environmental isolates. These results indicate that reactivation of dormant C. gattii infections can occur many years after the infectious agent was acquired elsewhere.

    View details for DOI 10.3201/eid1810.120068

    View details for PubMedID 23017442

  • Defect in regulatory B-cell function and development of systemic autoimmunity in T-cell Ig mucin 1 (Tim-1) mucin domain-mutant mice PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Xiao, S., Brooks, C. R., Zhu, C., Wu, C., Sweere, J. M., Petecka, S., Yeste, A., Quintana, F. J., Ichimura, T., Sobel, R. A., Bonventre, J. V., Kuchroo, V. K. 2012; 109 (30): 12105-12110

    Abstract

    Tim-1, a type I transmembrane glycoprotein, consists of an IgV domain and a mucin domain. The IgV domain is essential for binding Tim-1 to its ligands, but little is known about the role of the mucin domain, even though genetic association of TIM-1 with atopy/asthma has been linked to the length of mucin domain. We generated a Tim-1-mutant mouse (Tim-1(?mucin)) in which the mucin domain was deleted genetically. The mutant mice showed a profound defect in IL-10 production from regulatory B cells (Bregs). Associated with the loss of IL-10 production in B cells, older Tim-1(?mucin) mice developed spontaneous autoimmunity associated with hyperactive T cells, with increased production of IFN-? and elevated serum levels of Ig and autoantibodies. However, Tim-1(?mucin) mice did not develop frank systemic autoimmune disease unless they were crossed onto the Fas-mutant lpr mice on a C57BL/6 background. Tim-1(?mucin)lpr mice developed accelerated and fulminant systemic autoimmunity with accumulation of abnormal double-negative T cells and autoantibodies to a number of lupus-associated autoantigens. Thus, Tim-1 plays a critical role in maintaining suppressive Breg function, and our data also demonstrate an unexpected role of the Tim-1 mucin domain in regulating Breg function and maintaining self-tolerance.

    View details for DOI 10.1073/pnas.1120914109

    View details for Web of Science ID 000306992700050

    View details for PubMedID 22773818

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