STYK1/NOK functions in a ligand independent and constitutive fashion to provoke tumor formation and to be up-regulated in many types of cancer cells. However, how STYK1/NOK functions at the whole animal level is completely unknown. Here, we found that STYK1/NOK-transgenic (tg) mice spontaneously developed immunosuppressive B-CLL-like disease with generally shorter life spans. The phenotype of STYK1/NOK-induced B-CLL was typically heterogeneous, and most often, presented lymphadenectasis accompanied with hepatomegaly and/or splenomegaly. STYK1/NOK-tg mice also suffered reduced immune responses. The expanded CD5+CD19+ (B1) lymphocyte pool was detected within peripheral lymphoid organs. Analysis on GEO profile revealed that expression of STYK1/NOK were significantly up-regulated in primary human B-CLL. Inoculation of blood cells from sick STYK1/NOK-tg mice into immune-deficient recipients recaptured the B1 malignant phenotype. Our study demonstrated that STYK1/NOK transgenic mouse may serve as a useful model system for the developments of novel diagnosis and treatment of B-CLL.
Keywords: B lymphocyte; B1 cells; CLL; Lymphadenectasis; STYK1/NOK.
Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.