Research Group

  • Assoc. Prof. Anthony Chang, Principal applicant
  • Prof. Anita Chong, Co-applicant
  • Prof. Markus Clark, Co-applicant
  • Assist. Prof. James Chon, Collaborator
  • Prof. Michelle Josephson, Collaborator
  • Prof. Maryellen Giger, Collaborator
  • Mrs Natalya Kaverina, Research Technician


  • University of Chicago, Chicago, USA


  • Visualizing Inflammatory Cell Interactions in Human Transplant Kidneys

Kidney transplantation is the best therapy for end-stage renal disease. The waitlist for kidney allografts continually increases and in the United States in 2012 it exceeds 90,000 patients. Although acute rejection within the first year of transplantation occurs in fewer than 10% of kidney transplant patients, the overall long-term survival of the transplanted kidney has remained stable without significant improvement for several decades. Also, human polyomavirus infections are an important cause of kidney transplant failure. Interstitial inflammation that is characteristic of acute rejection looks similar in a kidney biopsy to the interstitial inflammation due to polyomavirus infection. We need to improve our knowledge about the immune responses in the transplant kidney to distinguish these two diagnoses and develop better therapies. We plan to analyze the inflammatory cells and their interactions in biopsies from human kidney transplants by a novel quantitative method with complementary 3- dimensional image construction. Currently, we know that B cells, T cells, and dendritic cells are present in acute rejection, but the relationship of these cells and their interactions are unknown. In samples of kidney transplant biopsies, we will identify the B, T or dendritic cells and measure the distances between these cells with computer-aided image analysis. This allows thousands of measurements between many different types of inflammatory cells. Our group has shown that certain T cells (follicular helper cells) interact closely with B cells in lupus patients with this autoimmune kidney disease. We expect similar findings in patients with acute rejection, particularly those with antibodies targeting human leukocytes antigens (HLA) of the transplant kidney. We are primarily focused on the immune mechanisms of acute rejection, but the comparisons with polyomavirus nephropathy may lead to better comprehension of these injury mechanisms and should improve our ability to diagnose and treat these diseases.

Progress Report
Final Report