Ivo Veletic, MD

ALT The causes of immune suppression, neutropenia, and anemia in CLL remain unclear. We found that exosomes derived from CLL cells – taken up by healthy monocytes, fibrocytes, and lymphocytes – alter gene/protein expression and suppress normal blood cell formation. These exosomes reprogram monocytes to mimic CLL-supportive cells, upregulate immune checkpoint proteins in T cells, and induce apoptosis and CD5 expression in normal B cells. RNA profiling showed that CLL exosomes carry RNAs promoting apoptosis, metabolism, proliferation, and PI3K–mTOR signaling. They also inhibit hematopoietic progenitor cell growth and impair monocyte-derived fibrocyte support. Our findings suggest CLL exosomes actively disrupt immune and hematopoietic function, contributing to disease progression.

ALT STAT3 activates the pentraxin 3 gene in chronic lymphocytic leukemia cells

ALT GLI1 activates pro-fibrotic pathways in myelofibrosis fibrocytes