ISSN: 2155-9899
Suhyeon Kim
Sungkyunkwan University, South Korea
Posters & Accepted Abstracts: J Clin Cell Immunol
Pellino (PELI1) 1 is highly conserved in the various species and contains C3HC4 RING motif in its C-terminal domains and catalyzes ubiquitin chains of several key molecules linked to lysine 48 (K48) or 63 (K63) in cell signaling pathway. PELI1 has been recently found to regulate Toll-like receptor (TLR) and T-cell receptor (TCR) signaling to NF-�ºB and thus contributes to the maintenance of self-tolerance and the production of pro-inflammatory cytokines. In addition, activation of B cell and T cell receptor-mediated signaling induces PELI1 expression and activation. However, their physiological roles in other cell types and cell signaling pathways remain unclear. We developed transgenic mice models to examine the molecular lesion caused by PELI1 gain-of-function. Constitutive expression of PELI1 resulted in ligand-independent hyperactivation of B cells and facilitated the development of a wide range of lymphoid tumors, with prominent B cell infiltration observed across multiple organs. PELI1 directly interacted with the oncoprotein B cell chronic lymphocytic leukemia (BCL6) and induced K63mediated BCL6 polyubiquitination. Furthermore, PELI1 expression levels positively correlated with BCL6 expression, and PELI1 overexpression was closely associated with poor prognosis in DLBCLs. Recently, we generated doxycycline-inducible human PELI1 transgenic mice. A major advantage of our mouse model is that the disease is inducible and can be induced at any stage of life, and the degree as well as the state of inflammation (acute, chronic, or batch wise) can be fine-tuned. We observed that the acute and chronic induction of PELI1 resulted in abnormal development and activation of peripheral immune system and could developed autoimmune disease and chronic inflammatory disease
Suhyeon Kim has completed her Master’s degree from Sungkyunkwan University and is currently a PhD candidate at the Sungkyunkwan University School of Medicine.
Email:suhyeon90514@gmail.com