Publications by authors named "Mike Vadi"
The T cell population size is stringently controlled before, during, and after immune responses, as improper cell death regulation can result in autoimmunity and immunodeficiency. RIPK1 is an important regulator of peripheral T cell survival and homeostasis. However, whether different peripheral T cell subsets show a differential requirement for RIPK1 and which programmed cell death pathway they engage in vivo remains unclear.
View Article and Find Full Text PDFArticle Synopsis
- Extracellular vesicles (EVs) play a crucial role in cell-to-cell communication, especially during regulated cell death (RCD), although their composition and function during different types of RCD were poorly understood until now.
- The study compared steady-state EVs (ssEVs) to EVs associated with cell death (cdEVs) produced from TNF-induced necroptosis, anti-Fas-induced apoptosis, and ML162-induced ferroptosis, revealing that cdEVs contain heightened protein levels and distinct biochemical properties.
- Notably, while all cdEVs had similarities in protein cargo, specific types like necEVs and apoEVs were linked to proteins related to ribosome biogenesis, contrasting with
Receptor-Interacting serine/threonine-Protein Kinase 1 (RIPK1) emerged as an important driver of inflammation and, consequently, inflammatory pathologies. The enzymatic activity of RIPK1 is known to indirectly promote inflammation by triggering cell death, in the form of apoptosis, necroptosis and pyroptosis. Small molecule Receptor-Interacting serine/threonine-Protein Kinase 1 inhibitors have therefore recently entered clinical trials for the treatment of a subset of inflammatory pathologies.
View Article and Find Full Text PDF