School of Biomedical Sciences cordially invites you to join the following seminar:

Speaker: Dr. Sangbum Park, Assistant Professor, Department of Medicine and Department of Pharmacology & Toxicology, Michigan State University
Talk Title: Dual lineages of Langerhans cells cooperate for immune barrier recovery after skin injury

Date: 12 June 2025 (Thursday)
Time: 4:00 pm – 5:00 pm
Venue: Seminar Room 1, G/F, Laboratory Block, 21 Sassoon Road
Host: Professor Rio Sugimura

Biography

Sangbum received B.S. in Animal Biotechnology and Ph.D. in Stem Cell Biology at the Seoul National University in South Korea. He completed his postdoctoral training with Dr. Valentina Greco in the Department of Genetics at Yale University. Sangbum is currently an Assistant Professor at Michigan State University (2020 - present).

Dr. Park focuses on understanding the principles of regeneration in the wound context that rebuild tissue de novo after injury. Dr. Park established a live cell imaging approach to study tissue repair in vivo and applied this new technology to determine how distinct cells of different fates coordinate their behaviors to promote re-epithelialization after injury. His ongoing research is investigating how crosstalk between epithelial cells and co-existing niche components, such as tissue-resident immune cells, contribute to effective homeostasis and wound repair.

Abstract

Tissue-resident immune cells in the skin provide a first line of defense against infections. Langerhans cells (LCs) in the epidermis act as sentinels by surveilling skin and presenting antigens in lymph nodes. While LCs maintain well-organized spatial distribution in healthy skin, the mechanisms governing their de novo reconstitution following tissue damage remain elusive. Through longitudinal tracking of LCs and their progenitor cells in live adult mice, we discovered that most activated LCs near wounds (eLCs) stay local and directly contribute to restoring LCs in injured tissue rather than migrating to lymphatics. Simultaneously, monocytes infiltrate the epidermis during wound repair and differentiate into additional LCs (mLCs) that remain long after healing. While the inhibition of Cxcr2 signaling impairs eLCs contribution, mLCs compensate for this deficiency. Our findings reveal fundamental mechanisms of immune barrier recovery through coordinated repopulation by distinct LC lineages in damaged skin.

All are welcome.