Publications by authors named "Wolf Steels"
Acute systemic inflammation critically alters the function of the immune system, often promoting myelopoiesis at the expense of lymphopoiesis. In the thymus, systemic inflammation results in acute thymic atrophy and, consequently, impaired T-lymphopoiesis. The mechanism by which systemic inflammation impacts the thymus beyond suppressing T-cell development is still unclear.
View Article and Find Full Text PDFThe 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
- Acute thymic atrophy occurs after type 1 inflammatory conditions like viral infections and sepsis, leading to cell death and affecting T cell development.
- Single-cell RNA sequencing identifies neonatal thymic-resident ILC1s as a distinct and immature group compared to those in other lymphoid organs, and exposure to certain cytokines (IL-12 and IL-18) promotes their rapid growth and migration.
- Type 1 inflammation not only causes thymic atrophy but also enhances the movement of these ILC1s to other areas like the liver and peritoneal cavity, indicating a potential role in immune responses.