American Association of Plastic Surgeons

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Immune Repertoire in Lymphedema: Characterizing the Dendritic Cell Subsets in a Lymphedema Mouse Model
Adana- Christine Campbell, MD, Arielle Roberts, DO, Bracha J Pollack, BA, Gopika Ashokan, MS, HyeungJu Park, PhD, Jinyeon Shin, MS, Yollanda Parisotto, PhD, Raghu Kataru, PhD, Chrysothemis Brown, MBBS, PhD, Babak J Mehrara, MD
Memorial Sloan Kettering Cancer Center, New York, NY, USA

Purpose: Secondary lymphedema (LE) is a chronic T-cell mediated disease. Clonal analysis of the CD4+ Tcells in clinical LE skin biopsies suggests that specific T-cell activating antigens contribute to the T-cell responses that are necessary for LE development. Thus, the aim of this study was to characterize the specific dendritic cell (DC) subset that dictates antigen presentation and ultimately T-cell fate in secondary lymphedema. Methods: We utilized a popliteal lymph node dissection (PLND) model of LE and analyzed the conventional DC (cDC) subsets in the ipsilateral, skin draining inguinal lymph node (LN) using Flow cytometry (Cytek Aurora) (n=7 per group). Briefly, LN tissues were minced to create single cell suspensions and flow analysis was performed for the expression of markers specific for conventional DC subsets; cDC1, cDC2A, and cDC2B. Results: Our results indicate that the cDC (CD11C+ MHCII+) population is significantly higher in the PLND-operated group when compared to non-operated controls (p<0.05). Flow analysis demonstrated a significant increase in the cDC2B population in the PLND model overall (p=0.004). Notably, expression of the co-stimulatory molecules, CD80 and CD86, which play an important role in regulating T-cell responses, was increased in this subset in the PLND group (p<0.0001). Conclusions: DC subsets as antigen targets have a unique therapeutic potential for altering T-cell responses. Here we provide preliminary evidence of a specific DC subset in LE using an established LE mouse model. This will enable future investigations into targeting the diversity of T-cell responses and antigen specificities in LE management.


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