International Keloid Symposium 2026

Dr. Tai-Lan Tuan is a member of the faculty at Department of Surgery, Keck School of Medicine, University of Southern California and the Saban Research Institute of Children’s Hospital Los Angeles. Dr. Tuan received her postdoctoral training in the area of Cell-ECM interactions from Dr. Fred Grinnell at the University of Texas Southwestern Medical Center at Dallas. The in vitro three dimensional fibrin matrix model of fibroplasia for wound healing was established in the early stage of her independent research career. Using the model system and in collaboration closely with her clinical and other colleagues, the molecular phenotype of keloid fibroblasts to include plasminogen activator inhibitor-1 (PAI-1) was discovered with evidence supporting the role PAI-1 in collagen accumulation (Am J. Pathol., 173(5):1311-25, 2008). Extending from the experience and established work, Dr. Tuan has taken a focused effort in the past several years to generate a clinically relevant and deliverable keloid-derived, plasma/fibrin-based skin equivalent animal model of keloid fibrosis that bridges the major gap of keloid translational research (Wound Repair Regen., 24(2):302-16, 2016). The model epitomizes the injury-repair environment in triggering and fostering keloid formation and the dynamic epidermal/dermal interactions which occur during disease development. The biological continuity of keloid genesis in the model system provides an accessible platform to elucidate the disease mechanism and test knowledge-based therapies. Dr. Tuan’s research has been supported by the National Institutes of Health (NIH), Department of Health and Human Services, USA.

Prof. Krueger’s group focuses on cutaneous inflammation and autoimmune mechanisms in human skin. Their research is fundamentally rooted in “bench-to-bedside” science, combining the clinical study of new medical therapeutics with laboratory research on relevant immunopathogenic mechanisms in human cells and tissues. The laboratory conducts clinical research on patients with psoriasis Vulgaris at The Rockefeller University Hospital. By combining novel immune-directed therapeutics with the large-scale study of gene expression, an approach called pharmacogenetics, the researchers seek to uncover the molecular pathways that cause pathogenic inflammation and regulate normal human immune responses. More experimental immunotherapeutics have been tested for psoriasis than for any other human inflammatory disease. Prof. Krueger’s group has pioneered several successful treatments, including some that act on T cells. One of these therapies counteracts specific inflammatory cytokines; another involves a type of ultraviolet light with immunomodulatory properties. Prof. Krueger’s research in healthy skin has shown that a previously unknown population of dendritic cells exists alongside macrophages in the skin. Other recent work by members of the lab has shown that a newly discovered immune cell, Th17, plays a central role in psoriasis and could serve as a target for future therapies. This T cell subset is regulated by IL-23, a protein shown by the group to be upregulated in psoriasis. IL-23 antagonism has produced major improvements in psoriasis, suggesting a new class of therapeutics. And by investigating the contribution of activated T lymphocytes, Krueger has found that psoriasis may be induced by tissue-infiltrating T lymphocytes, which trigger keratinocytes into a physiologically regulated wound repair pathway of hyperplasia and altered differentiation.