Translocator Protein Deficiency Promotes Splenomegaly with Extramedullary Hematopoiesis after Sepsis

This study investigates the role of translocator protein (TSPO) in splenic immune responses following sepsis using a mouse cecal ligation and puncture (CLP) model. Bulk RNA sequencing of spleen tissue collected 17 days after sham or CLP surgery revealed that TSPO deficiency promotes splenomegaly characterized by red pulp expansion, enhanced erythropoiesis, and reduced immune responses. Gene expression and deconvolution analyses indicated decreased lymphocyte signatures and increased erythroblast and megakaryocyte signatures in TSPO knockout mice. These findings suggest that TSPO plays a critical role in maintaining splenic immune homeostasis after sepsis.