Honors & Awards

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

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.


    Maitland Cottage Home, Cape Town

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

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


    Bay Area, California, USA


Work Experience

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


    VA Palo Alto Health Care System

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


    Brigham and Women's Hospital


All Publications

  • 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
  • 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


    Homing of murine dendritic epidermal T cells (DETCs) from the thymus to the skin is regulated by specific trafficking receptors during late embryogenesis. Once in the epidermis, V?3?1 TCR DETCs are maintained through self-renewal and participate in wound healing. GPR15 is an orphan G protein-linked chemoattractant receptor involved in the recruitment of regulatory T cells to the colon. Here we show that GPR15 is highly expressed on fetal thymic DETC precursors and on recently recruited DETCs, and mediates the earliest seeding of the epidermis, which occurs at the time of establishment of skin barrier function. DETCs in GPR15(-/-) mice remain low at birth, but later participation of CCR10 and CCR4 in DETC homing allows DETCs to reach near normal levels in adult skin. Our findings establish a role for GPR15 in skin lymphocyte homing and suggest that it may contribute to lymphocyte subset targeting to diverse epithelial sites.

    View details for DOI 10.1002/eji.201444628

    View details for PubMedID 24838826

  • 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


    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


    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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