Honors & Awards

  • Stanford Graduate Fellowship, Stanford University (2012)

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


Journal Articles

  • 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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